By Kirsty Jackson (@kjjscience)
Every field of study has, what we call, a model organism. Scientists carry out experiments using the model organism and use it as a base for assumptions about other related organisms. Model organisms tend to be small, grow and reproduce quickly, have small genomes and are easily manipulated in the lab. In the animal world the mouse is a commonly used model, in plants we have Arabidopsis thaliana, and the fungal world has Neurospora crassa. In this blog I would like to explain how Neurospora crassa claimed it status as the Kate Moss of the fungal world.
Neurospora crassa (I pronounce this Neuros-pora) is a small filamentous fungus, or mould, classed within the ascomycetes. It was first noted in 1843 in Paris, where bakeries were plagued by a mould that produced vast crops of orange powdery spores known as conidia. It was named as Monilia sitophila and was found on carbohydrate-rich food and the remains of burnt vegetation. It wasn’t until 1927 that it was placed into the Neurospora genus by Bernard O. Dodge and Cornelius L. Shear after observing the sexual fruiting bodies.
N. crassa has a predominant haploid (n) life stage, meaning that for the majority of its life cycle it only has one copy of its genome. It briefly undergoes a diploid (2n) stage before meiosis in the sexual cells. In 1939, N. crassa found acclaim in the world of genetics when all four products of meiosis were recovered. Subsequent studies of meiosis in N. crassa revealed the segregation of alleles and the crossing over of chromatids (the arms of a chromosome).
The haploid nature of N. crassa cultures made looking for phenotypes caused by genetic mutation easier than in diploid model organisms also used in the 1940s, such as fruit fly (Drosophila melanogaster). N. crassa can also be easily cultured in the lab on agar plates with very little nutrients in the media. Two scientists, George Beadle and Edward Tatum used these features of N. crassa to identify mutants that required additional nutrients in their growth media, showing that genetic mutations were directly responsible for biochemistry within the cells (see video). At the time it was still believed that genes were only responsible for developmental planning, such as wing shape and eye colour, and not biochemical processes such as the ability to make vitamins and metabolites.
Advances in lab techniques during the 1940s and 1950s saw an emergence of a Wild-type strain and a population that could be used in recombination with other strains to map genetic mutations to the chromosomes, which were identified by Barbara McClintock in 1945. This, as well as a way to preserve stocks in suspended animation enabled the accumulation and maintenance of large numbers of N. crassa strains within laboratories for genetic and biochemical studies.
Unfortunately, N. crassa was quickly usurped by the bacteria Escherichia coli as the model organism for genetics and biochemical studies. However, as E. coli is a prokaryotic organism it is unable to answer many Eukaryote-specific questions such as how circadian clocks worked and how different of cell types arose. The Fungal Genetics Stock Centre created in 1961 provided ready access to mutant strains and a worldwide collection of over 4000 N. crassa strains (useful for studying natural genetic diversity). Combined with the collaborative nature of the N. crassa research community, N. crassa became a broadly studied organism once more. However, once again N. crassa was pushed to the sidelines as work on Yeast (Saccharomyces cerevisiae) bloomed and was used to help answer the Eukaryote-specific biochemical and molecular biology problems.
Yet like a phoenix from the ashes, N. crassa rose again. A number of scientists stayed with N. crassa, through a sense of loyalty or because they had just invested too much into their research to change. It was then that N. crassa became the model of the higher filamentous fungi. It was met with some resistance at first by the traditional N. crassa researchers; but after the annual Neurospora meeting was widened to include other filamentous fungi, and renamed the Fungal Genetics Conference, it became clear that interests were shared. With the wealth of knowledge already built up on N. crassa, it was a great base for fungal studies and the understanding of other fungal species. The genome sequence was completed in 2003 and now a wealth of computational resources exists as well as a selection of knockout mutants (generated in 2006) held at the Fungal Genetics Stock Centre.
Like most model organisms, N. crassa has its downsides. Being an ascomycete it cannot be used to answer questions about the mushroom/toadstool development of the basidiomyctes. Nor can it answer specific pathogenicity questions for fungi that are pathogens of plants or animals. However, N. crassa will remain a vital tool for the common fungal elements and for general cell biology.
About the author: Kirsty Jackson is a PhD student at the John Innes Centre, Norwich. She is studying rhizobial and mycorrhizal symbioses with legumes and loves all things fungi! When she isn’t in the lab she is involved with organising science outreach events. Follow her on twitter (@kjjscience)
Davis, R.H. and Perkins, D.D. (2002) Neurospora: a model of a model microbes. Nature Reviews: Genetics 3 7-13
Colot, H.V. et al (2006) A high-throughput gene knockout procedure for Neurospora reveals functions for multiple transcription factors. PNAS 103 (27) 10352-10357
James E. Galagan. et al (2003) The genome sequence of the filamentous fungus Neurospora crassa. Nature 442 859-868
Images and videos of Neurospora from Prof. N. Louise Glass’s lab in Berkley, CA. http://glasslab.berkeley.edu/gallery/cool-neurospora-images-and-videos
Images and movies from Prof Nick Read’s Fungal Cell Biology group http://www.fungalcell.org/images-and-movies
Fungal Genetics Stock Centre http://www.fgsc.net/