Neurospora crassa – the Ultimate Genetic Puppet

By: Nils Nelson

Since the rise of evolutionary theory stemming from Darwin in the 1840s the mystery of the exact processes of inheritance and evolution has begun to unfold. Though it was not until 1970 that the first organism’s genome was sequenced, there was a trail of key developments in proving genes existence and purpose that resulted in the now immense field of genetics and our understanding of biology today.

In 1941 George Beadle and Edward Tatum published a paper on the relationship of genes to enzymes in the fungus Neurospora crassa first reported in French bakeries in 1843 (Beadle, Tatum. 1941). This became known as the one gene-one hypothesis, which later became the one gene-one polypeptide theory. This discovery became the foundation for solving genetic code and brought the fields of biochemistry and genetics together. Beadle and Tatum proved their hypothesis by first mutating sexual spores of the fungus with x-rays and ultraviolet light then isolating mutated spores. Next they selectively bred compatible strains with mutants then grow the resulting genetic offspring on nutrient deprived agar growth medium. Carefully they added the precursors for a specific nutrient and track when an enzyme was not present to convert the pre product molecules. This led them to be able to narrow down the defect of a single gene to the absence of a single enzyme. Today there is a current project attempting to produce a knockout mutant strain of N. crassa mutant for each gene in the genome.

This was not the end of the road for scientific insights provided by N. crassa. The ability to determine the phenotype of all four products of individual meiosis granted insight into the function of genetic recombination in all eukaryotes and became principle evidence for the adaptive function of recombination and out crossing (Murray, 1960). This fungus gave us the first evidence for gene conversion which is a correction mechanism during genetic combination of combatable partners. Another genetic protection system first reported in N. crassa was repeat-induced suppression in which haploid genomes are scanned for duplicate genes, and if found, are polarized by a released mutagen which acts to silence or methylate a genetic element. Studies on N. crassa additionally proved that fungi were eukaryotic which developed our understanding metabolic pathways in all eukaryotes (Davis 2000). Lastly, on the scientific glory list from this fungus is that it was involved with the discovery of mitochondria in 1953. Today, N. crassa is still studied extensively for discoveries in genetics, epigenetics, circadian rhythms, and molecular processes. It is also used in education (Dunlap 1999; Dunlap 2000; Dunlap 2008). This fungus has earned the title of a model organism due to its history of study and usefulness. Some of these useful attributes include a largely haploid life cycle, fast life cycle (10 days), genetic simplicity, wide distribution, and availability of strains. Some of my favorites include “frost”, “cum”, “it pokes along”, and “microcycle blastoconidiation”. The entire genome for N. crassa was sequenced in 2003.

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Photos: Fungal Genetics Stock Center.

Neuro life cycle

Source: Wikipedia

wild Neurospora

Jacobson David. Stanford University.

N. crassa is a fungi in the class ascomycota. It reproduces both asexually via structures called conidia and sexually via structures called asci. N. crassa ascospores are found to only germinate upon a heat treatment of atleast 60C. This has to do with its life strategy in ecology. N. crassa grows primarily in circum boreal regions, although it has recently been found in temperate region. It occurs on wood and vegetation after forest fires where it appears as a red to orange dust or cotton appearance. Although in lab N. crassa has been studied exensively, much is still unknown about its functions in nature. Due of its relationship with heat it became a bane for bakeries and remains a common contaminant today. N. crassa remains one of the most important organisms of genetic study to date in addition to a slew of other findings and developments in biology. Not only did this fungus vastly increase our understanding of fungi it provided us with key insights into the functions of higher eukaryotes such as ourselves. It is amazing to me how open ended the possibilities for us to increase our biological understanding with fungi. We have the ability now to deeply investigate and study these organisms with the advent of sterile environments, gene sequencing, staining, computing etc. Further inquiry into this comparatively untouched field will become increasingly significant to progress in biology.


Beadle, G. W., and E. L. Tatum, 1941 Genetic Control of Biochemical Reactions in Neurospora. Proc Natl Acad Sci U S A 27: 499-506.

Davis, R., 2000 Neurospora: Contributions of a Model Organism. Oxford University Press, New York.

Davis, R., 2000 Neurospora: Contributions of a Model Organism. Oxford University Press, New York.

Dunlap, J. C., 1999 Molecular bases for circadian clocks. Cell 96: 271-290.

Dunlap, J. C., 2008 Salad days in the rhythms trade. Genetics 178: 1-13.

Murray, N. E. 1960. Complementation and recombination between Methionine-2 alleles in Neurospora crassa. Heredity 15:207–217.


Gavric Olivera. Images of Neurospora Morphological Mutants in Culture. Fungal Genetics Stock Center.

Neurospora Crassa Life Cycle. Wikipedia.

Jacobson David. Stanford University.

Aspergillus niger: not your everyday mold

By Jasmine Zamora

When many people think of fungi, they first envision beautiful fruiting bodies that grow out of the damp grass and soil.  However, there is a much darker side of the kingdom fungi that can cause sickness and death.  The members of the Aspergillus genus do not grow on recently rained-on terrain, nor do they need a specific temperature to grow in.  These are molds, most familiarly Aspergillus niger, can in some cases cause disease in humans, animals and plants.Aspergillus

Aspergillus niger isn’t as notoriously dangerous as Aspergillus fumigatus, which is the most prevalent airborne fungal pathogen (Latgé 1999).  However, Aspergillus niger contains toxins that can make people with weak immune systems become very sick and can sometimes result in death.  These toxins can be inhaled by humans, most commonly people who work around plants or peat, and can cause a lung disease called Aspergillosis, which has infected over 300,000 people worldwide (Keir 2013).  Aspergillus niger is not one of those that are so deadly, but can definitely cause sickness and allergic reactions.  Aspergillus niger is an asexual saprophytic fungus that can grow on dead leaves, stored grain, compost piles and other decaying vegetation.  A. niger is a very thermotolerant fungus that can thrive in freezing conditions and very hot weather (Metzger 2008).  It produces its spores on an asexual structure called the conidium.  The spores can be inhaled when simply working with anything A. niger has colonized.

Aspergillus niger contains several toxins, some harmless and others harmful to certain people.  The main toxins it contains are malformin C, and ochratoxin A.  A. niger can be as beneficial as it is harmful, though.  Through fermentation, it can produce useful enzymes that can be used in the production of corn syrup, Beano, wine and cider (Rajkumar 2010).

Fortunately, most people can handle the inhalation of a moderate amount of A. niger spores.  Aspergillus spores are in the air we breathe almost everywhere we go.  It is those who suffer from leukemia, HIV or AIDS, severe fungal allergies and other immune deficiencies that could become very sick to the intake of A. niger spores (Bartholomew 2009).  There has actually been a case where a 70 year old man had to have his foot amputated because there was a “painful black ‘gangrenous appearing’ mass on his foot.  “Tissue samples showed not only branching hyphae, but dark pigmented fungal fruiting heads with double sterigmata in which Aspergillus niger was identified” (  This may be a case of a sickly man that was just unfortunate enough to come into contact with A. niger, but the so-called “harmless” fungi can effect healthy people in rare cases.  Otomycosis, an ear infection that can be very painful, can be caused by Aspergillus niger.  Allergic reactions can be severe when an individual that is very allergic to fungi.  “When inhaled, A. niger can cause hypersensitivity reactions such as asthma and allergic alveolitis” (  This is uncommon, but nearly fatal if the wrong person became infected.

A. niger can also affect plants, such as onions and tomatoes. Small animals, such as mice and chicks were fed moldy soybeans with A. niger on them, and the subjects subsequently died after digestion ( Onions are a common plant that A. niger likes to inhabit, causing spoilage and can then result in economic loss in farming communities.  Mangoes, grapes and tomatoes are also victims of the pathogen, as well as 34 other genera of plants.  Lastly, A. niger can cause the rotting of wood and other hard surfaces. Wood surfaces have been found softening or deteriorating because of the contamination of A. niger. There have also been reports of A. niger effecting very random substrates such as polyvinyl acetate, polyester-type polyurethanes, and even English style crumpets.

Aspergillus niger does not discriminate when it comes to what it wmoldants to contaminate.  However, this very durable fungus is nothing to be worried about, unless you have a weak immune system or have a sensitive allergy to fungi, or if you are a mouse.  There are also remedies that can be taken if one contracts Otomycosis or another common fungal infection.  There are many other more harmful fungi that are in the same family (A. fumigatus) to be worried about, so be sure you don’t inhale too many A. niger spores, and don’t eat heavily molded fruits that are covered in a black substance, and you should be fine.

 Works Cited

Anonymous. 1997. Aspergillus niger Final Risk Assessment. Biotechnology program under toxic substances control act (TSCA) U.S. Environmental Protection Agency U.S.A. 3171.

Corrigan. (October 15, 2009). Aspergillus niger. In Encyclopedia of Life. Retrieved January 28, 2014, from

Keir, G. J., Garfield, B., Hansell, D. M., Loebinger, M. R., Wilson, R., Renzoni, E. A., & Maher, T. M. (2013). Cyclical caspofungin for chronic pulmonary aspergillosis in sarcoidosis. Thorax, thoraxjnl-2013.

Latgé, J. P. (1999). Aspergillus fumigatus and aspergillosis. Clinical microbiology reviews, 12(2), 310-350.

Metzger, B. (November 16, 2008). Aspergillus niger . In Mushroom Observer. Retrieved January 28, 2014, from

Paul, R., Singh, V., Tyagi, R., Singh, A., & Dubey, D. (2010). Micro-Elements work for the growth and total soluble protein production in Aspergillus niger at different concentrations. Journal of Pure and Applied Microbiology, 4, 293-296.

Sutton, D. A. 2005. Aspergillus niger.  Retrieved February 10, 2014. from:

SCIMAT.  Aspergillus niger fungus. Retrieved February 10, 2014. from: