Information

1.4.9.12: Fungal Structure and Habitats - Biology

1.4.9.12: Fungal Structure and Habitats - Biology



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Learning Objectives

  • Describe the common structures of fungi
  • Identify common habitats of fungi

Cell Structure and Function

Fungi are eukaryotes, and as such, have a complex cellular organization. As eukaryotes, fungal cells contain a membrane-bound nucleus. The DNA in the nucleus is wrapped around histone proteins, as is observed in other eukaryotic cells. A few types of fungi have structures comparable to bacterial plasmids (loops of DNA); however, the horizontal transfer of genetic information from one mature bacterium to another rarely occurs in fungi. Fungal cells also contain mitochondria and a complex system of internal membranes, including the endoplasmic reticulum and Golgi apparatus.

Unlike plant cells, fungal cells do not have chloroplasts or chlorophyll. Many fungi display bright colors arising from other cellular pigments, ranging from red to green to black. The poisonous Amanita muscaria (fly agaric) is recognizable by its bright red cap with white patches (Figure 1). Pigments in fungi are associated with the cell wall and play a protective role against ultraviolet radiation. Some fungal pigments are toxic.

Like plant cells, fungal cells have a thick cell wall. The rigid layers of fungal cell walls contain complex polysaccharides called chitin and glucans. Chitin, also found in the exoskeleton of insects, gives structural strength to the cell walls of fungi. The wall protects the cell from desiccation and predators. Fungi have plasma membranes similar to other eukaryotes, except that the structure is stabilized by ergosterol: a steroid molecule that replaces the cholesterol found in animal cell membranes. Most members of the kingdom Fungi are nonmotile. Flagella are produced only by the gametes in the primitive Phylum Chytridiomycota.

Habitats

Although fungi are primarily associated with humid and cool environments that provide a supply of organic matter, they colonize a surprising diversity of habitats, from seawater to human skin and mucous membranes. Chytrids are found primarily in aquatic environments. Other fungi, such as Coccidioides immitis, which causes pneumonia when its spores are inhaled, thrive in the dry and sandy soil of the southwestern United States. Fungi that parasitize coral reefs live in the ocean. However, most members of the Kingdom Fungi grow on the forest floor, where the dark and damp environment is rich in decaying debris from plants and animals. In these environments, fungi play a major role as decomposers and recyclers, making it possible for members of the other kingdoms to be supplied with nutrients and live.


Albugo: Habitat, Symptoms and Reproduction | Mastigomycotina

In this article we will discuss about Albugo. After reading this article you will learn about: 1. Habit and Habitat of Albugo 2. Symptoms of Albugo 3. Vegetative Structure 4. Reproduction 5. Biological Specialization or Physiological Specialization 6. Control Measures.

  1. Habit and Habitat of Albugo
  2. Symptoms of Albugo
  3. Vegetative Structure of Albugo
  4. Reproduction in Albugo
  5. Biological Specialization or Physiological Specialization in Albugo
  6. Control Measures of Albugo

1. Habit and Habitat of Albugo:

Albugo (derived from a Latin word means white), the only genus of family Albuginaceae is represented by more than 25 species. It is an obligate parasite distributed all over the world.

In India about 18 species of Albugo have been reported which attacks mostly crucifers like turnip, mustard, radish, cabbage, cauliflower etc. However, it has also been reported on some members of family Asteraceae (Composite, Convolvulaceae and Chenopodiaceae).

2. Symptoms of Albugo:

The disease caused by Albugo is commonly known as white rust because it appears in the form of shiny, white, smooth irregular patches (pustules) or blisters on the leaves, stems and other aerial parts of the plant. The pustules are initially formed on the lower surface of the leaf but in several cases they may be present on both the surfaces (Fig. 1 A).

With this several other effects are also produced. Increase in the size of the cells (hypertrophy) and organs takes place. It results in the formation of large galls on the various parts of the host (Fig. 1 B-D). Severe infection causes proliferation of the lateral buds, discoloration of flowers, malformation of floral parts and sterile gynoecium.

3. Vegetative Structure of Albugo:

Thallus is eucarpic and mycelial. Hyphae are intercellular, coenocytic, aseptate and profusely branched(Fig. 2 B). Cell wall is composed of fungal cellulose. The protoplasm contains a large number of nuclei distributed in the cytoplasm.

Reserve food material is in the form of oil drops and glycogen bodies. Some mycelium is intracellular in the form of knob-like haustoria for the absorption of food material from the host cells. The ultrastructure of haustoria is studied by Berlin and Bowen (1964).

It can be differentiated into two parts:

The cytoplasm of the head of haustorium is densely packed with mitochondria, ribosomes, endoplasmic reticulum and lipid inclusions but nuclei are absent.

The base of the haustorium is surrounded by a collar like oeath which is an extension of the host cell wall. Between the haustorium and the host plasma membrane is an encapsulation. Within the plasma membrane of the haustorium lomasomes are more numerous than in the intercellular hyphae.

4. Reproduction in Albugo:

The fungus reproduces both by asexual and sexual methods (Fig. 5, 6).

Asexual Reproduction:

The asexual reproduction takes place by conidia, condiosporangia or zoosporangia. They are produced on the sporangiophores. Under suitable conditions the mycelium grows and branches rapidly.

After attaining a certain age of maturity, it produces a dense mat like growth just beneath the epidermis of the host (Fig. 2 D). These hyphae produce, at right angles to the epidermis are short, thick walled, un-branched and club shaped. These are the sporangiophores or conidiophores.

They form a solid, palisade like layer beneath the epidermis (Fig. 2 A-D). They are thick walled on lateral sides and thin walled at tip. The sporangiophores contain dense cytoplasm and about a dozen nuclei. After reaching a certain stage of maturity, the apical portion of sporangiophore gets swollen and is ready is cut off a sporangium or conidium (Fig. 2E).

The sporangia are produced at the tip by abstraction method. A Deeping constriction appears below the swollen (fig 2. F)end and results in the formation of first sporangium. A second sporangium is similarly formed from the tip just beneath the previous one (Fig. 2 G).

This process is repeated several times. The new nuclei migrates from mycelium to cytoplasm and are used in the formation of another sporangium or conidium. Thus along chain of sporangia or conidia is formed above each sporangiophore in basipetal succession. (youngest at the base and oldest at the tip) (Fig. 2 H).

The sporangia or conidia are spherical, smooth, hyaline and multinucleate structures. The walls between them fuse to form a gelatinous disc-like structure called disjunctor or separation disc or intercalary disc. (Fig. 2 G).

It tends to hold the sporangia together. The continued growth and production of sporangia exerts a pressure upon the enveloping epidermis. Which is firstly raised up but finally ruptured exposing the underlying sours containing white powdery dust of multinucleate sporangia or conidia (Fig. 2 A, 3).

The separation discs are dissolved by water, and the sporangia are set free. They are blown away in the air by wind or washed away by rain water under suitable environmental conditions and falling on a suitable host, sporangia germinates with in 2 or 3 hours. The sporangia germinate directly or indirectly depending on temperature conditions.

1. Direct Germination:

At high temperature and comparative dry conditions the sporangium germinates directly. It gives rise to a germ tube which in-fact the host tissue through stoma or through an injury in the epidermis (Fig. 2 I, P).

2. Indirect Germination:

In the presence of moisture and low temperature (10°C) the sporangium germinates indirectly i.e., it behaves like zoosporangium and produces zoospores. It absorbs water, swells up, and its contents divide by cleaving into 5-8 polyhedral parts (Fig. 2 J) depending upon the nuclei present in it. Each part later on rounds up and metamorphoses into zoospore (Fig. 2 K, L). A papilla is developed on one side which later burst and liberates the zoospores.

The zoospores are uninucleate, slightly concavo-convex and biflagellate. The flagella are attached laterally near the vacuole. Of the two flagella one is of whiplash type and the other tinsel type (Fig. 2M). After swimming for some time in water, they settle down on the host.

They retract their flagella, secrete a wall and undergo a period of encystment (Fig. 2 N). On germination, they put out a short germ tube which enters the host through stomata (Fig. 2 O, P) or again infects the healthy plants.

Sexual Reproduction:

It takes place when the growing season comes to an end. The mycelium penetrates into the deeper tissues of the host. The sexual reproduction is highly oogamous type. The antheridium and oogonium develops deeper in the host tissue in close association within the intercellular spaces.

Its formation is externally indicated by hypertrophy. The antheridium and oogonium are formed near each other on hyphal branches. They are terminal in position, however, intercalary oogonia also occur, though rarely.

It is elongated and club shaped structure. It is multinucleate (6-12 nuclei) but only one nucleus remains functional at the time of fertilization in C. candidus. However, in C. bliti and C. portulace it is multinucleate at the time of fertilization and all the nuclei (nearly 100) remain functional. It is paragynous i.e., laterally attached to the oogonium (Fig. 4 A-C). It is separated by a cross wall from the rest of the male hyphae.

It is spherical and multinucleate containing as many as 65 to 115 nuclei. All nuclei are evenly distributed throughout the cytoplasm (Fig. 4 A-C). As the oogonium reaches towards the maturity the contents of the oogonium get organised into an outer peripheral region of periplasm and the inner dense central region of ooplasm or oosphere or the egg (Fig. 4 D-G). The ooplasm and periplasm are separated by a plasma membrane.

The nuclei in the oogonium divides mitotically. The first mitotic division takes place before the organization of the periplasm and oosplasm (Fig. 4 E). After the organization, all the nuclei of the ooplasm, except one, migrate to the periplasm forming a ring and undergo second mitotic division. They divide in such a manner that one pole of each spindle is in ooplasm and the other in the periplasm (Fig. 4 E).

At the end of the division one daughter nucleus of each spindle goes to the oosplasm and other in periplasm (Fig. 4 F). However, at the time of maturity, all nuclei disintegrate, except single functional nucleus (Fig. 4 G). On the basis of functional nuclei in ooplasm,” Albugo is divided into following groups:

The number of functional egg nucleus in ooplasm is one. It is represented by C. tragopogonis, C. candidus, C. evolvuli etc.

The number of functional eggs in ooplasm is many. It is represented by C. bliti, C. portulacae etc.

It has been observed that in C. portulacae and C. bliti nearly 60 nuclei accumulate in the ooplasm and after fertilization they fuse with the male nuclei. However, in C. tragopogonis about a hundred female nuclei are present in the oosphere, but only one in functional. The rest of the nuclei disintegrate before fertilization.

Before fertilization a deeply staining mass of cytoplasm, (Fig. 4 H) appears almost in the centre of the ooplasm. This is called coenocentrum. It persists only up to the time of fertilization. The functional female nucleus attracted towards it and becomes attached to a point near it.

The oogonium develops a papilla like out growth at the point of contact with the antheridium. This is called as receptive papilla (Fig. 4 G). Soon it disappears, and the antheridium develops a fertilization tube.

It penetrates through receptive papilla, oogonial wall and periplasm and finally reaches upto the ooplasm (Fig. 4 H, L). It carries a single male nucleus. Its tip ruptures to discharge the male nucleus near the female nucleus. Ultimately the male nucleus fuses with the female nucleus (karyogamy).

The oospore alongwith the fusion nucleus is called oospore (Fig. 4 J). In C. tragopogonis and C. candidus, one male functional nucleus fuses with one female functional nucleus. So, the oospore is uninucleate. However, in C. portulaceae and C. bliti, oospore is multinulceate. consisting of nearly 60 functional nuclei.

The same number of functional male nuclei are discharged by the fertilization tube. Both male and female nuclei fuse, and the oospore produced in these species in multinucleate. Such oospore is called a compound oospore.

The oospore on maturity secretes a two to three layered wall (Fig. 4 J-L). The outer layer is thick, warty or tuberculated and represents the exospore. The inner layer is thin and culled the endospore.

Germination of oospore:

With the secretion of the wall, the zygotic nucleus divides repeatedly to form about 32 nuclei. The first division is meiotic. At this stage the oospore undergoes a long period of rest until unfavorable conditions are over. Meanwhile its host tissues disintegrate leaving the oospore free. After a long period of rest the oospore germinates. Its nuclei divide mitotically and large number of nuclei are produced.

A small amount of cytoplasm gathers around each nucleus. Protoplasm undergoes segmentation and each segment later on rounds up and metamorphoses into a zoomeiospre or zoospore (Fig. 4 O). The exospore is ruptured and the endospore comes out as a thin vesicle (Fig. 4 M). The zoospores move out into the thin vesicle which soon perishes to liberate the zoospores.

However, Vanterpool (1959) reported that oospore forms a short exit or germ tube which ends in a thin vesicle. According to Stevens (1899), Sansome and Sansome (1974), the thallus of Albugo is diploid and the meiosis occurs in gametangla i.e., Antheridia and oogomia. Zygotic nucleus divides only mitotically and not meiotically.

Germination of Zoospore:

The zoospores are reniform (kidney shaped) and biflagellate. Of the two Safe flagella, long one is of whiplash type and short one is of tinsel type (Fig. 4 O). The zoospores after swimming for sometime encyst and germinate by a germ tube which reinfects the host plant (Fig. 4 O, P, Q).

5. Biological Specialization or Physiological Specialization in Albugo:

In Albugo, it has been observed that a species for e.g., A. Candida attacks only the members of family Brassicaceae (Cruciferae) but not others. It has also been observed that A. Candida infects only one host e.g., Brassica but it does not infect the other host i.e., radish. This means that the A. Candida obtained from different host are not the same and therefore, have to be named differently.

Thus the species should be divided into croups below species level. These are called biological forms or physiological forms. These biological forms ire specialised in parasitism, therefore, the phenomenon is called as biological specialization or physiological -specialization.

Some common species of Albugo with their hosts are:

(i) A. candia (= C. candidus) — Brassica, turnip, cabbage, Raphnus, Capsella, Eruca saliva.


Importance of fungi

Fungi are very important for a number of reasons worldwide. Mushrooms, truffles and yeast have a significant place in the food and alcohol industries as sources of food and in the process of fermentation. They are also used in the production of antibiotics.

Fungi are one of the most important decomposers of dead plant material and the recycling of nutrients back into ecosystems. If nutrients were not recycled, a habitat would become infertile and struggle to support life. On the flip side, all around the world fungi can be problematic for farmers because they can infect and decompose crops.

Many fungi, known as mycorrhizae, live in close association with the roots of plants and actually help them to absorb more nutrients. The vast majority of plants depend on help from fungi to successfully compete with neighbouring plants for nutrients.


Biology

The natural history of malaria involves cyclical infection of humans and female Anopheles mosquitoes. In humans, the parasites grow and multiply first in the liver cells and then in the red cells of the blood. In the blood, successive broods of parasites grow inside the red cells and destroy them, releasing daughter parasites (&ldquomerozoites&rdquo) that continue the cycle by invading other red cells.

The blood stage parasites are those that cause the symptoms of malaria. When certain forms of blood stage parasites (gametocytes, which occur in male and female forms) are ingested during blood feeding by a female Anopheles mosquito, they mate in the gut of the mosquito and begin a cycle of growth and multiplication in the mosquito. After 10-18 days, a form of the parasite called a sporozoite migrates to the mosquito&rsquos salivary glands. When the Anopheles mosquito takes a blood meal on another human, anticoagulant saliva is injected together with the sporozoites, which migrate to the liver, thereby beginning a new cycle.

Thus the infected mosquito carries the disease from one human to another (acting as a &ldquovector&rdquo), while infected humans transmit the parasite to the mosquito, In contrast to the human host, the mosquito vector does not suffer from the presence of the parasites.

The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver (if untreated) and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect red blood cells . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites&rsquo multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito&rsquos stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites, which make their way to the mosquito&rsquos salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle.

Human Factors And Malaria

Biologic characteristics and behavioral traits can influence an individual&rsquos risk of developing malaria and, on a larger scale, the intensity of transmission in a population.

Where does malaria transmission occur?

For malaria transmission to occur, conditions must be such so that all three components of the malaria life cycle are present:

  • Anopheles mosquitoes, which able to feed on humans humans, and in which the parasites can complete the &ldquoinvertebrate host&rdquo half of their life cycle
  • Humans. who can be bitten by Anopheles mosquitoes, and in whom the parasites can complete the &ldquovertebrate host&rdquo half of their life cycle
  • Malaria parasites.

In rare cases malaria parasites can be transmitted from one person to another without requiring passage through a mosquito (from mother to child in "congenital malaria" or through transfusion, organ transplantation, or shared needles.)

Climate

Climate is a key determinant of both the geographic distribution and the seasonality of malaria. Without sufficient rainfall, mosquitoes cannot survive, and if not sufficiently warm, parasites cannot survive in the mosquito.

Anopheles lay their eggs in a variety of fresh or brackish bodies of water, with different species having different preferences. Eggs hatch within a few days, with resulting larvae spending 9-12 days to develop into adults in tropical areas. If larval habitats dry up before the process is completed, the larvae die if rains are excessive, they may be flushed and destroyed. Life is precarious for mosquito larvae, with most perishing before becoming adults.

Life is usually short for adult mosquitoes as well, with temperature and humidity affecting longevity. Only older females can transmit malaria, as they must live long enough for sporozoites to develop and move to the salivary glands. This process takes a minimum of nine days when temperatures are warm (30°C or 86°F) and will take much longer at cooler temperatures. If temperatures are too cool (15°C or 59°F for Plasmodium vivax, 20°C or 68°F for P. falciparum), development cannot be completed and malaria cannot be transmitted. Thus, malaria transmission is much more intense in warm and humid areas, with transmission possible in temperate areas only during summer months.

In warm climates people are more likely to sleep unprotected outdoors, thereby increasing exposure to night-biting Anopheles mosquitoes. During harvest seasons, agricultural workers might sleep in the fields or nearby locales, without protection against mosquito bites.

Anopheles Mosquitoes

The types (species) of Anopheles present in an area at a given time will influence the intensity of malaria transmission. Not all Anopheles are equally efficient vectors for transmitting malaria from one person to another. Those species that are most prone to bite humans are the most dangerous, as bites inflicted on animals that cannot be infected with human malaria break the chain of transmission. If the mosquito regularly bites humans, the chain of transmission is unbroken and more people will become infected. Some species are biologically unable to sustain development of human malaria parasites, while others are readily infected and produce large numbers of sporozoites (the parasite stage that is infective to humans).

Many of the most dangerous species bite human indoors. For these species insecticide treated mosquito nets and indoor residual spray (whereby the inner walls of dwellings are coated with a long-lasting insecticide) are effective interventions. Both of these interventions require attention to insecticide resistance, which will evolve if the same insecticide is used continuously in the same area.

Humans

Biologic characteristics (inborn and acquired) and behavioral traits can influence an individual&rsquos malaria risk and, on a larger scale, the overall malaria ecology.

Parasites

Characteristics of the malaria parasite can influence the occurrence of malaria and its impact on human populations, for example:

  • Areas where P. falciparum predominates (such as Africa south of the Sahara) will suffer more disease and death than areas where other species, which tend to cause less severe manifestations, predominate
  • P. vivax and P. ovale have stages (&ldquohypnozoites&rdquo) that can remain dormant in the liver cells for extended periods of time (months to years) before reactivating and invading the blood. Such relapses can result in resumption of transmission after apparently successful control efforts, or can introduce malaria in an area that was malaria-free
  • P. falciparum (and to a lesser extent P. vivax) have developed strains that are resistant to antimalarial drugs. Such strains are not uniformly distributed. Constant monitoring of the susceptibility of these two parasite species to drugs used locally is critical to ensure effective treatment and successful control efforts. Travelers to malaria-risk areas should use for prevention only those drugs that will be protective in the areas to be visited.

Plasmodium falciparum predominates in Africa south of the Sahara, one reason why malaria is so severe in that area.

Animal Reservoirs

A certain species of malaria called P. knowlesi has recently been recognized to be a cause of significant numbers of human infections. P. knowlesi is a species that naturally infects macaques living in Southeast Asia. Humans living in close proximity to populations of these macaques may be at risk of infection with this zoonotic parasite.

Areas Where Malaria Is No Longer Endemic

Malaria transmission has been eliminated in many countries of the world, including the United States. However, in many of these countries (including the United States) Anopheles mosquitoes are still present. Also, cases of malaria still occur in non-endemic countries, mostly in returning travelers or immigrants (&ldquoimported malaria&rdquo). Thus the potential for reintroduction of active transmission of malaria exists in many non-endemic parts of the world. All patients must be diagnosed and treated promptly for their own benefit but also to prevent the reintroduction of malaria.

Genetic Factors

Biologic characteristics present from birth can protect against certain types of malaria. Two genetic factors, both associated with human red blood cells, have been shown to be epidemiologically important. Persons who have the sickle cell trait (heterozygotes for the abnormal hemoglobin gene HbS) are relatively protected against P. falciparum malaria and thus enjoy a biologic advantage. Because P. falciparum malaria has been a leading cause of death in Africa since remote times, the sickle cell trait is now more frequently found in Africa and in persons of African ancestry than in other population groups. In general, the prevalence of hemoglobin-related disorders and other blood cell dyscrasias, such as Hemoglobin C, the thalassemias and G6PD deficiency, are more prevalent in malaria endemic areas and are thought to provide protection from malarial disease.

Persons who are negative for the Duffy blood group have red blood cells that are resistant to infection by P. vivax. Since the majority of Africans are Duffy negative, P. vivax is rare in Africa south of the Sahara, especially West Africa. In that area, the niche of P. vivax has been taken over by P. ovale, a very similar parasite that does infect Duffy-negative persons.

Other genetic factors related to red blood cells also influence malaria, but to a lesser extent. Various genetic determinants (such as the &ldquoHLA complex,&rdquo which plays a role in control of immune responses) may equally influence an individual&rsquos risk of developing severe malaria.

Acquired Immunity

Acquired immunity greatly influences how malaria affects an individual and a community. After repeated attacks of malaria a person may develop a partially protective immunity. Such &ldquosemi-immune&rdquo persons often can still be infected by malaria parasites but may not develop severe disease, and, in fact, frequently lack any typical malaria symptoms.

In areas with high P. falciparum transmission (most of Africa south of the Sahara), newborns will be protected during the first few months of life presumably by maternal antibodies transferred to them through the placenta. As these antibodies decrease with time, these young children become vulnerable to disease and death by malaria. If they survive repeated infections to an older age (2-5 years) they will have reached a protective semi-immune status. Thus in high transmission areas, young children are a major risk group and are targeted preferentially by malaria control interventions.

In areas with lower transmission (such as Asia and Latin America), infections are less frequent and a larger proportion of the older children and adults have no protective immunity. In such areas, malaria disease can be found in all age groups, and epidemics can occur.

Anemia in young children in Asembo Bay, a highly endemic area in western Kenya. Anemia occurs most between the ages of 6 and 24 months. After 24 months, it decreases because the children have built up their acquired immunity against malaria (and its consequence, anemia).

Mother and her newborn in Jabalpur Hospital, State of Madhya Pradesh, India. The mother had malaria, with infection of the placenta.

Pregnancy and Malaria

Pregnancy decreases immunity against many infectious diseases. Women who have developed protective immunity against P. falciparum tend to lose this protection when they become pregnant (especially during the first and second pregnancies). Malaria during pregnancy is harmful not only to the mothers but also to the unborn children. The latter are at greater risk of being delivered prematurely or with low birth weight, with consequently decreased chances of survival during the early months of life. For this reason pregnant women are also targeted (in addition to young children) for protection by malaria control programs in endemic countries.

Behavioral Factors

Human behavior, often dictated by social and economic reasons, can influence the risk of malaria for individuals and communities. For example:

  • Poor rural populations in malaria-endemic areas often cannot afford the housing and bed nets that would protect them from exposure to mosquitoes. These persons often lack the knowledge to recognize malaria and to treat it promptly and correctly. Often, cultural beliefs result in use of traditional, ineffective methods of treatment.
  • Travelers from non-endemic areas may choose not to use insect repellent or medicines to prevent malaria. Reasons may include cost, inconvenience, or a lack of knowledge.
  • Human activities can create breeding sites for larvae (standing water in irrigation ditches, burrow pits)
  • Agricultural work such as harvesting (also influenced by climate) may force increased nighttime exposure to mosquito bites
  • Raising domestic animals near the household may provide alternate sources of blood meals for Anopheles mosquitoes and thus decrease human exposure
  • War, migrations (voluntary or forced) and tourism may expose non-immune individuals to an environment with high malaria transmission.

Human behavior in endemic countries also determines in part how successful malaria control activities will be in their efforts to decrease transmission. The governments of malaria-endemic countries often lack financial resources. As a consequence, health workers in the public sector are often underpaid and overworked. They lack equipment, drugs, training, and supervision. The local populations are aware of such situations when they occur, and cease relying on the public sector health facilities. Conversely, the private sector suffers from its own problems. Regulatory measures often do not exist or are not enforced. This encourages private consultations by unlicensed, costly health providers, and the anarchic prescription and sale of drugs (some of which are counterfeit products). Correcting this situation is a tremendous challenge that must be addressed if malaria control and ultimately elimination is to be successful.

Protective Effect of Sickle Cell Trait Against Malaria

The sickle cell gene is caused by a single amino acid mutation (valine instead of glutamate at the 6th position) in the beta chain of the hemoglobin gene. Inheritance of this mutated gene from both parents leads to sickle cell disease and people with this disease have shorter life expectancy. On the contrary, individuals who are carriers for the sickle cell disease (with one sickle gene and one normal hemoglobin gene, also known as sickle cell trait) have some protective advantage against malaria. As a result, the frequencies of sickle cell carriers are high in malaria-endemic areas.

CDC&rsquos birth cohort studies (Asembo Bay Cohort Project in western Kenya) conducted in collaboration with the Kenya Medical Research Institute allowed an investigation into this issue. It was found that that the sickle cell trait provides 60% protection against overall mortality. Most of this protection occurs between 2-16 months of life, before the onset of clinical immunity in areas with intense transmission of malaria.

Graph of survival curves (&ldquosurvival function estimates&rdquo) of children without any sickle cell genes (HbAA), children with sickle cell trait (HbAS), and children with sickle cell disease (HbSS). Those who had the sickle cell trait (HbAS) had a slight survival advantage over those without any sickle cell genes (HbAA), with children with sickle cell disease (HbSS) faring the worst.

Reference: Protective Effects of the Sickle Cell Gene Against Malaria Morbidity and Mortality. Aidoo M, Terlouw DJ, Kolczak MS, McElroy PD, ter Kuile FO, Kariuki S, Nahlen BL, Lal AA, Udhayakumar V. Lancet 2002 359:1311-1312.

Anopheles Mosquitoes

Malaria is transmitted to humans by female mosquitoes of the genus Anopheles. Female mosquitoes take blood meals for egg production, and these blood meals are the link between the human and the mosquito hosts in the parasite life cycle. The successful development of the malaria parasite in the mosquito (from the &ldquogametocyte&rdquo stage to the &ldquosporozoite&rdquo stage) depends on several factors. The most important is ambient temperature and humidity (higher temperatures accelerate the parasite growth in the mosquito) and whether the Anopheles survives long enough to allow the parasite to complete its cycle in the mosquito host (&ldquosporogonic&rdquo or &ldquoextrinsic&rdquo cycle, duration 9 to 18 days). In contrast to the human host, the mosquito host does not suffer noticeably from the presence of the parasites.

Diagram of Adult Female Mosquito

Map of the world showing the distribution of predominant malaria vectors

Anopheles freeborni mosquito pumping blood
Larger Picture

General Information

There are approximately 3,500 species of mosquitoes grouped into 41 genera. Human malaria is transmitted only by females of the genus Anopheles. Of the approximately 430 Anopheles species, only 30-40 transmit malaria (i.e., are &ldquovectors&rdquo) in nature. The rest either bite humans infrequently or cannot sustain development of malaria parasites.

Geographic Distribution

Anophelines are found worldwide except Antarctica. Malaria is transmitted by different Anopheles species in different geographic regions. Within geographic regions, different environments support a different species.

Anophelines that can transmit malaria are found not only in malaria-endemic areas, but also in areas where malaria has been eliminated. These areas are thus at risk of re-introduction of the disease.

Life Stages

Like all mosquitoes, anopheles mosquitoes go through four stages in their life cycle: egg, larva, pupa, and adult. The first three stages are aquatic and last 7-14 days, depending on the species and the ambient temperature. The biting female Anopheles mosquito may carry malaria. Male mosquitoes do not bite so cannot transmit malaria or other diseases. The adult females are generally short-lived, with only a small proportion living long enough (more than 10 days in tropical regions) to transmit malaria.

Adult females lay 50-200 eggs per oviposition. Eggs are laid singly directly on water and are unique in having floats on either side. Eggs are not resistant to drying and hatch within 2-3 days, although hatching may take up to 2-3 weeks in colder climates.

Larvae

Mosquito larvae have a well-developed head with mouth brushes used for feeding, a large thorax, and a segmented abdomen. They have no legs. In contrast to other mosquitoes, Anopheles larvae lack a respiratory siphon and for this reason position themselves so that their body is parallel to the surface of the water.

Top: Anopheles Egg note the lateral floats.
Bottom: Anopheles eggs are laid singly.

Larvae breathe through spiracles located on the 8th abdominal segment and therefore must come to the surface frequently.

The larvae spend most of their time feeding on algae, bacteria, and other microorganisms in the surface microlayer. They do so by rotating their head 180 degrees and feeding from below the microlayer. Larvae dive below the surface only when disturbed. Larvae swim either by jerky movements of the entire body or through propulsion with the mouth brushes.

Larvae develop through 4 stages, or instars, after which they metamorphose into pupae. At the end of each instar, the larvae molt, shedding their exoskeleton, or skin, to allow for further growth.

Anopheles Larva. Note the position, parallel to the water surface.

The larvae occur in a wide range of habitats but most species prefer clean, unpolluted water. Larvae of Anopheles mosquitoes have been found in fresh- or salt-water marshes, mangrove swamps, rice fields, grassy ditches, the edges of streams and rivers, and small, temporary rain pools. Many species prefer habitats with vegetation. Others prefer habitats that have none. Some breed in open, sun-lit pools while others are found only in shaded breeding sites in forests. A few species breed in tree holes or the leaf axils of some plants.

Pupae

The pupa is comma-shaped when viewed from the side. This is a transitional stage between larva and adult. The pupae does not feed, but undergoes radical metamorphosis. The head and thorax are merged into a cephalothorax with the abdomen curving around underneath. As with the larvae, pupae must come to the surface frequently to breathe, which they do through a pair of respiratory trumpets on the cephalothorax. After a few days as a pupa, the dorsal surface of the cephalothorax splits and the adult mosquito emerges onto the surface of the water.

The duration from egg to adult varies considerably among species and is strongly influenced by ambient temperature. Mosquitoes can develop from egg to adult in as little as 7 days but usually take 10-14 days in tropical conditions.

Anopheles Adults. Note (bottom row) the typical resting position.

Adults

Like all mosquitoes, adult anopheles have slender bodies with 3 sections: head, thorax and abdomen.

The head is specialized for acquiring sensory information and for feeding. The head contains the eyes and a pair of long, many-segmented antennae. The antennae are important for detecting host odors as well as odors of aquatic larval habitats where females lay eggs. The head also has an elongate, forward-projecting proboscis used for feeding, and two sensory palps.

The thorax is specialized for locomotion. Three pairs of legs and a single pair of wings are attached to the thorax.

The abdomen is specialized for food digestion and egg development. This segmented body part expands considerably when a female takes a blood meal. The blood is digested over time serving as a source of protein for the production of eggs, which gradually fill the abdomen.

Anopheles mosquitoes can be distinguished from other mosquitoes by the palps, which are as long as the proboscis, and by the presence of discrete blocks of black and white scales on the wings. Adult Anopheles can also be identified by their typical resting position: males and females rest with their abdomens sticking up in the air rather than parallel to the surface on which they are resting.

Adult mosquitoes usually mate within a few days after emerging from the pupal stage. In some species, the males form large swarms, usually around dusk, and the females fly into the swarms to mate. The mating habitats of many species remain unknown.

Males live for about a week, feeding on nectar and other sources of sugar. Females will also feed on sugar sources for energy but usually require a blood meal for the development of eggs. After obtaining a full blood meal, the female will rest for a few days while the blood is digested and eggs are developed. This process depends on the temperature but usually takes 2-3 days in tropical conditions. Once the eggs are fully developed, the female lays them then seeks blood to sustain another batch of eggs.

The cycle repeats itself until the female dies. Females can survive up to a month (or longer in captivity) but most do not live longer than 1-2 weeks in nature. Their chances of survival depend on temperature and humidity, but also upon their ability to successfully obtain a blood meal while avoiding host defenses.

Female Anopheles dirus feeding

Factors Involved in Malaria Transmission and Malaria Control

Understanding the biology and behavior of Anopheles mosquitoes can aid in designing appropriate control strategies. Factors that affect a mosquito&rsquos ability to transmit malaria include its innate susceptibility to Plasmodium, its host choice, and its longevity. Long-lived species that prefer human blood and support parasite development are the most dangerous. Factors that should be taken into consideration when designing a control program include the susceptibility of malaria mosquitoes to insecticides and the preferred feeding and resting location of adult mosquitoes.

Preferred Sources for Blood Meals

One important behavioral factor is the degree to which an Anopheles species prefers to feed on humans (anthropophily) or animals such as cattle (zoophily). Anthrophilic Anopheles are more likely to transmit the malaria parasites from one person to another. Most Anopheles mosquitoes are not exclusively anthropophilic or zoophilic many are opportunistic and feed upon whatever host is available. However, the primary malaria vectors in Africa, An. gambiae and An. funestus, are strongly anthropophilic and, consequently, are two of the most efficient malaria vectors in the world.

Life Span

Once ingested by a mosquito, malaria parasites must undergo development within the mosquito before they are infectious to humans. The time required for development in the mosquito (the extrinsic incubation period) takes 9 days or longer, depending on the parasite species and the temperature. If a mosquito does not survive longer than the extrinsic incubation period, then she will not be able to transmit any malaria parasites.

It is not possible to measure directly the life span of mosquitoes in nature, but many studies have indirectly measured longevity by examination of their reproductive status or via marking, releasing, and recapturing adult mosquitoes. The majority of mosquitoes do not live long enough to transmit malaria, but some may live as long as three weeks in nature. Though evidence suggests that mortality rate increases with age, most workers estimate longevity in terms of the probability that a mosquito will live one day. Usually these estimates range from a low of 0.7 to a high of 0.9. If survivorship is 90% daily, then a substantial proportion of the population would live longer than 2 weeks and would be capable of transmitting malaria. Any control measure that reduces the average lifespan of the mosquito population will reduce transmission potential. Insecticides thus need not kill the mosquitoes outright, but may be effective by limiting their lifespan.

Patterns of Feeding and Resting

Most Anopheles mosquitoes are crepuscular (active at dusk or dawn) or nocturnal (active at night). Some Anopheles mosquitoes feed indoors (endophagic) while others feed outdoors (exophagic). After blood feeding, some Anopheles mosquitoes prefer to rest indoors (endophilic) while others prefer to rest outdoors (exophilic). Biting by nocturnal, endophagic Anopheles mosquitoes can be markedly reduced through the use of insecticide-treated bed nets (ITNs) or through improved housing construction to prevent mosquito entry (e.g., window screens). Endophilic mosquitoes are readily controlled by indoor spraying of residual insecticides. In contrast, exophagic/exophilic vectors are best controlled through source reduction (destruction of larval habitats).

Insecticide Resistance

Insecticide-based control measures (e.g., indoor spraying with insecticides, ITNs) are the principal way to kill mosquitoes that bite indoors. However, after prolonged exposure to an insecticide over several generations, mosquitoes, like other insects, may develop resistance, a capacity to survive contact with an insecticide. Since mosquitoes can have many generations per year, high levels of resistance can arise very quickly. Resistance of mosquitoes to some insecticides has been documented within a few years after the insecticides were introduced. There are over 125 mosquito species with documented resistance to one or more insecticides. The development of resistance to insecticides used for indoor residual spraying was a major impediment during the Global Malaria Eradication Campaign. Judicious use of insecticides for mosquito control can limit the development and spread of resistance, particularly via rotation of different classes of insecticides used for control. Monitoring of resistance is essential to alert control programs to switch to more effective insecticides.

Susceptibility/Refractoriness

Some Anopheles species are poor vectors of malaria, as the parasites do not develop well (or at all) within them. There is also variation within species. In the laboratory, it has been possible to select for strains of An. gambiae that are refractory to infection by malaria parasites. These refractory strains have an immune response that encapsulates and kills the parasites after they have invaded the mosquito&rsquos stomach wall. Scientists are studying the genetic mechanism for this response. It is hoped that some day, genetically modified mosquitoes that are refractory to malaria can replace wild mosquitoes, thereby limiting or eliminating malaria transmission.

Malaria Parasites

Malaria parasites are micro-organisms that belong to the genus Plasmodium. There are more than 100 species of Plasmodium, which can infect many animal species such as reptiles, birds, and various mammals. Four species of Plasmodium have long been recognized to infect humans in nature. In addition there is one species that naturally infects macaques which has recently been recognized to be a cause of zoonotic malaria in humans. (There are some additional species which can, exceptionally or under experimental conditions, infect humans.)

Ring-form trophozoites of P. falciparum in a thin blood smear.

Ring-form trophozoites of P. vivax in a thin blood smear.

Trophozoites of P. ovale in a thin blood smear.

Band-form trophozoites of P. malariae in a thin blood smear.

Schizont and ring-form trophozoite of P. knowlesi in a thin blood smear.


Discussion

Based on a mesocosm experiment of arbuscular mycorrhizal and ectomycorrhizal artificial plant communities, we examined how mycorrhizal types determine plant–soil microbiota feedbacks. Previous studies have generally reported negative feedbacks in arbuscular mycorrhizal plant species and positive feedbacks in ectomycorrhizal species 1,8,9 , and Bennett et al. 9 emphasized that species-specific feedbacks could play a more important role than mycorrhizal type match/mismatch. We found that, in a multi-species community context, the direction and strength of feedbacks depend critically on mycorrhizal type match/mismatch. When seedlings colonize forests dominated by the matching mycorrhizal type, arbuscular mycorrhizal plant species tend to exhibit negative or neutral feedbacks and ectomycorrhizal plant species do neutral or positive feedbacks (Fig. 3). In contrast, when seedlings colonize forests dominated by the matching versus mismatching mycorrhizal type, both arbuscular mycorrhizal and ectomycorrhizal species exhibit neutral or positive feedbacks as a consequence of mycorrhizal type matching (Fig. 4). Our results suggest, when these within- and across-mycorrhizal type feedbacks occur simultaneously in natural forest, ectomycorrhizal plant species may show more positive feedbacks than arbuscular mycorrhizal plant species do. Consequently, the assembly of a temperate tree seedling community may be shaped by a combination of variable feedbacks within the same mycorrhizal guilds and positive feedbacks across different mycorrhizal guilds.

This study also revealed that the root-associated fungal community shared between saplings and seedlings may be associated with the observed patterns of plant–soil feedbacks. Specifically, for the ectomycorrhizal plant community, seedlings’ fungal symbiont acquisition and the spatial structuring of belowground fungal communities may account for the pattern that ectomycorrhizal seedlings generally performed better under the matching resident forests than under the mismatching forests (Figs. 5 and 6). We propose that the observed effects of mycorrhizal type matching on resident–seedling feedbacks may have resulted from four non-mutually exclusive mechanisms: first, more spatially extended and temporally prolonged infection of seedling roots by matching fungal communities than by mismatching ones second, detrimental effects of incompatible mycorrhizal fungi for seedlings when grown with mismatched saplings third, access to a larger soil nutrient pool made available by compatible fungal networks than by incompatible networks 19,20,21 and fourth, more active transport of nutrients from resource-rich regions of mycelial networks to resource-poor areas 22 via more structured hyphal networks provided by matching symbioses. The analyses of fungal communities within the mesocosms (Figs. 5 and 6) are consistent with all these possibilities. Nevertheless, the use of the internal transcribed spacer (ITS) region in the molecular analysis might have resulted in a low detection rate of arbuscular mycorrhizal fungi (see ref. 26 for more), and it is likely that arbuscular mycorrhizal fungal communities would have displayed spatial structuring when analyzed using DNA markers specific to arbuscular mycorrhizal fungi. While our results suggest the roles of mycorrhizal fungal communities and their belowground networks as a potential driver of plant–soil feedbacks, detailed mechanisms underlying the link between fungal symbiont acquisition and plant−soil feedbacks require further investigation.

Our approach to determining plant–soil feedbacks is different from previous research in two important ways. First, previous studies either focused on the effects of live soil inocula associated with a single resident plant species on conspecific or heterospecific seedlings (i.e., plant competition-free conditions 9,11,27 ) or on the effects of one resident plant species on another in the presence of resident-seedling competition 20,28,29,30 . Our study assembled plant−soil communities on identical substrates of a set area, naturally and in situ at a field site, and for a known period of time, and then measured seedling growth responses under conditions in which both plant competition and mycorrhizal networks were allowed to develop. These features made it possible to examine feedbacks in more realistic, multi-species plant communities. Second, most field studies have used fungicide to test for the potential effects of soil pathogens 2,3,7,9 , but such chemical applications were necessarily confounded with possible reductions of soil mycorrhizal fungi, which could also act as key agents of feedbacks 18,25 . By combining a factorial experiment with follow-up sequencing, we were able to quantify the similarities in root-associated fungal community composition between resident trees and seedlings as a potential key agent of plant−soil feedbacks. Our findings show that the biological effect of plant−soil interactions can be placed into a broader community context, whereas it has typically been only observed in pairwise interactions.

It is necessary to note, however, some caveats of our study. First, there are some methodological limitations in our soil handling, which might potentially bias the estimation of feedbacks (see Methods for mode detail). Second, at the conditioning phase of the experiment, we chose to use mycorrhizal saplings (collected from natural forests by a local nursery) over using cultured mycorrhizal inocula. Therefore, it is possible that diverse soil biota other than mycorrhizal fungi might have driven the observed feedbacks. For instance, bacteria, soil micro-arthropods, and nematodes are also known as potential key agents of plant−soil feedbacks 2,4,10,31 , so whether they could explain the direction and strength of feedbacks observed in our study is still an open question. Third, we did not account for variation in plant species composition and richness in the mesocosm designs. For the sake of experimental feasibility and tractability, we assembled two artificial tree communities from each type to test for matching/mismatching feedbacks. If we are to confirm the generality of the findings, further studies must be undertaken to assess how the direction and strength of feedbacks differ depending on the compositions of the arbuscular mycorrhizal and ectomycorrhizal plant species used to build the experimental mesocosms. This is important because research has shown that plant–soil feedbacks can not only affect plant community structure 4,7,10 (but see ref. 29 ) but also be affected by plant community structure 32,33 . Fourth, seedlings used in this study might have exceeded the stage susceptible to soil pathogens which might have caused underestimation of negative soil biota effects 34 , and this possibility cannot be ruled out given the scarcity of pathogens detected in our study (Supplementary Figure 4). A related issue is that such pathogens are known to deactivate under high light intensity, potentially reducing the efficacy of pathogen-mediated negative feedbacks. Despite our efforts to simulate the natural forest environment by controlling for light availability experienced by seedlings (see Experimental design described in Methods), our field experiment might have been performed in environments with higher light intensity compared to previous studies. Previous experiments and ours may thus differ in several aspects potentially influencing the functioning of plant–soil microbiota feedbacks (e.g., light intensity, soil fertility 24,35,36,37 ), and hence the results of feedbacks should be interpreted with caution (see Supplementary Table 5 for the soil chemical profiles for our experiment).

Understanding plant–soil feedbacks in mixed-species communities and evaluating how contrasting plant mycorrhizal types shape plant−soil feedbacks are critical to predicting plant community dynamics and succession. Our findings show that the effects of plant–soil feedbacks on seedling community assembly can be modulated by mycorrhizal type match/mismatch, and such matching effects may emerge as a community-scale process in which the networks of interactions formed by soil microbiota influence the outcome of seedling community assembly. Plant–soil feedback theory predicts that stronger negative feedbacks are more likely to stabilize species coexistence within the same mycorrhizal fungal guilds (i.e., within an arbuscular mycorrhizal plant community or an ectomycorrhizal plant community), whereas more positive feedbacks observed across different mycorrhizal types are more likely to allow specific mycorrhizal plant guilds to become dominant in a forest (in our case, arbuscular mycorrhizal plant dominated forest or ectomycorrhizal plant dominated forest). Our findings may provide clues to simultaneously explain why different tree species of the same mycorrhizal type can coexist in a natural temperate forest, and why ectomycorrhizal plant communities (but not arbuscular mycorrhizal plant communities) often dominate in late-successional temperate forest.

Although the idea that mycorrhizal type is a significant predictor of plant community succession is not new 8,38 , it has not been tested experimentally at the community level. This study is a first step toward contrasting arbuscular mycorrhizal and ectomycorrhizal plant–soil feedbacks in a multi-species context and highlights the importance of simultaneously examining arbuscular mycorrhizal and ectomycorrhizal plant communities. As mycorrhizal types have been linked to plant nutritional acquisition strategies, soil properties, and nutrient cycling 24,25 , they provide a useful approach for an understanding of feedbacks at the ecosystem level. To develop a more comprehensive understanding of plant community assembly, future studies need to quantitatively evaluate the roles of both arbuscular mycorrhizal and ectomycorrhizal fungi 15,38,39 as well as the diversity and biomass of mycorrhizal, endophytic, and pathogenic fungi in plant root systems 16,40 in association with various abiotic factors 41 . Incorporating such complexities of real belowground plant–soil interactions will be an avenue for better predicting plant community dynamics.


Fungal Biology in the Origin and Emergence of Life

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  • Publisher: Cambridge University Press
  • Online publication date: February 2013
  • Print publication year: 2013
  • Online ISBN: 9781139524049
  • DOI: https://doi.org/10.1017/CBO9781139524049
  • Subjects: Plant Sciences, Life Sciences, Evolutionary Biology

Email your librarian or administrator to recommend adding this book to your organisation's collection.

Book description

The rhythm of life on Earth includes several strong themes contributed by Kingdom Fungi. So why are fungi ignored when theorists ponder the origin of life? Casting aside common theories that life originated in an oceanic primeval soup, in a deep, hot place, or even a warm little pond, this is a mycological perspective on the emergence of life on Earth. The author traces the crucial role played by the first biofilms – products of aerosols, storms, volcanic plumes and rainout from a turbulent atmosphere – which formed in volcanic caves 4 billion years ago. Moore describes how these biofilms contributed to the formation of the first prokaryotic cells, and later, unicellular stem eukaryotes, highlighting the role of the fungal grade of organisation in the evolution of higher organisms. Based on the latest research, this is a unique account of the origin of life and its evolutionary diversity to the present day.

Reviews

'In a wonderful introduction to this wide and exciting subject, and ensuring accessibility to non-specialist readers, key features of fungal biology are introduced, as is current thinking on the beginnings of the solar system, the formation of the Earth and its Moon, and the possible origins of the building blocks of life, including panspermia, the ET origin of life on earth. Central in this thought provoking book is a consideration of the definition of what is life, from the philosophical to the rigidly scientific. This definition is key to deciding on what was LUCA, the last universal common ancestor. Current views on this are well reviewed, critically analysed and dissected. A fascinating read, a myco-centric version of the origin of the eukaryotes, firmly dismissing the animal biased theories.'

J. L. Faull - Birkbeck, University of London

'Fungi and animals share a deep Precambrian root from which our unicellular ancestors diverged more than one billion years ago. This common beginning is evident when we look at similarities between fungus and animal at the level of genes and proteins, as well as the grander disjunction between both groups of eukaryotes and every other form of life on earth. Mycologist David Moore details the evolutionary history of the fungi in his new book and its relationship to the origins and subsequent development of life on land. This rich and compelling story provides a crucial mycological perspective on some of the biggest questions in modern biology.'

Nicholas Money - Miami University, Ohio

'Why are fungi ignored when theorists ponder the origins of life on Earth? This book provides a refreshing mycological perspective on this fascinating question. Moore presents well-supported arguments for the origin and emergence of life on this planet. This quite accessible book will change many a mind on this topic.'

Adele Kleine Source: chicagobotanic.org

'In this new and challenging book, David [Moore] aims to place fungi centre-stage in the origin and evolution of life … carefully researched and argued … original and stimulating thesis.'

'This wonderful, refreshing take on origins-of-life studies reviews the present state of affairs, including the missing elements of fungal biology. Every biologist in this field needs to read this book. Moore provides a highly intelligent and reasoned assessment of the role of fungal biology in the discussion of the origins and early evolution of life on Earth. Highly recommended.'

P. K. Strother Source: Choice

'… pitched at a level where a very wide range of readers should feel rewarded by the many sage views clearly expressed, and the fair-handed discussions of multiple conflicting hypotheses about the subject matter … This volume is particularly recommended to those mycologists who focus on issues of fungal phylogeny.'


Protist Life Cycles and Habitats

Protists live in a wide variety of habitats, including most bodies of water, as parasites in both plants and animals, and on dead organisms.

Learning Objectives

Describe the habitats and life cycles of various protists

Key Takeaways

Key Points

  • Slime molds are categorized on the basis of their life cycles into plasmodial or cellular types, both of which end their life cycle in the form of dispersed spores.
  • Plasmodial slime molds form a single-celled, multinucleate mass, whereas cellular slime molds form an aggregated mass of separate amoebas that are able to migrate as a unified whole.
  • Slimes molds feed primarily on bacteria and fungi and contribute to the decomposition of dead plants.

Key Terms

  • haploid: of a cell having a single set of unpaired chromosomes
  • sporangia: an enclosure in which spores are formed (also called a fruiting body)
  • plasmodium: a mass of cytoplasm, containing many nuclei, created by the aggregation of amoeboid cells of slime molds during their vegetative phase
  • diploid: of a cell, having a pair of each type of chromosome, one of the pair being derived from the ovum and the other from the spermatozoon

Life Cycle of Slime Molds

Protist life cycles range from simple to extremely elaborate. Certain parasitic protists have complicated life cycles and must infect different host species at different developmental stages to complete their life cycle. Some protists are unicellular in the haploid form and multicellular in the diploid form, which is a strategy also employed by animals. Other protists have multicellular stages in both haploid and diploid forms, a strategy called alternation of generations that is also used by plants.

Plasmodial slime molds

The slime molds are categorized on the basis of their life cycles into plasmodial or cellular types. Plasmodial slime molds are composed of large, multinucleate cells and move along surfaces like an amorphous blob of slime during their feeding stage. The slime mold glides along, lifting and engulfing food particles, especially bacteria. Upon maturation, the plasmodium takes on a net-like appearance with the ability to form fruiting bodies, or sporangia, during times of stress. Meiosis produces haploid spores within the sporangia. Spores disseminate through the air or water to potentially land in more favorable environments. If this occurs, the spores germinate to form amoeboid or flagellate haploid cells that can combine with each other and produce a diploid zygotic slime mold to complete the life cycle.

Plasmodial slime mold life cycle: Haploid spores develop into amoeboid or flagellated forms, which are then fertilized to form a diploid, multinucleate mass called a plasmodium. This plasmodium is net-like and, upon maturation, forms a sporangium on top of a stalk. The sporangium forms haploid spores through meiosis, after which the spores disseminate, germinate, and begin the life cycle anew. The brightly-colored plasmodium in the inset photo is a single-celled, multinucleate mass.

Cellular slime molds

The cellular slime molds function as independent amoeboid cells when nutrients are abundant. When food is depleted, cellular slime molds aggregate into a mass of cells that behaves as a single unit called a slug. Some cells in the slug contribute to a 2–3-millimeter stalk, which dries up and dies in the process. Cells atop the stalk form an asexual fruiting body that contains haploid spores. As with plasmodial slime molds, the spores are disseminated and can germinate if they land in a moist environment. One representative genus of the cellular slime molds is Dictyostelium, which commonly exists in the damp soil of forests.

Cellular slime mold life cycle: Cellular slime molds may engage in two forms of life cycles: as solitary amoebas when nutrients are abundant or as aggregated amoebas (inset photo) when nutrients are scarce. In aggregate form, some individuals contribute to the formation of a stalk, on top of which sits a fruiting body full of spores that disseminate and germinate in the proper moist environment.

Habitats of Various Protists

There are over 100,000 described living species of protists. Nearly all protists exist in some type of aquatic environment, including freshwater and marine environments, damp soil, and even snow. Paramecia are a common example of aquatic protists. Due to their abundance and ease of use as research organisms, they are often subjects of study in classrooms and laboratories. In addition to aquatic protists, several protist species are parasites that infect animals or plants and, therefore, live in their hosts. Amoebas can be human parasites and can cause dysentery while inhabiting the small intestine. Other protist species live on dead organisms or their wastes and contribute to their decay. Approximately 1000 species of slime mold thrive on bacteria and fungi within rotting trees and other plants in forests around the world, contributing to the life cycle of these ecosystems.


1.4.9.12: Fungal Structure and Habitats - Biology

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