Carolyn Elya

Huge thanks to the efforts of some pretty fun guys and gals that made this collaborative effort possible: @hyphaltip@genomic.social, @Lovettbr@arthropod.social, @kasson_wvu@bird.makeup, @debivort@drosophila.social, plus several folks not on the 'don (Angie, Emily, Ann & Henrik!). Go Entomophthorales! (n/n)

In fact, E. muscae’s genome is 1.03 Gb and more than 90% of this is repetitive. Imagine trying to put together a puzzle accurately where 90% of the pieces are identical!

We found that the large genome size of E. muscae is caused by a large expansion of TE’s (specifically Ty3 retrotransposons), which apparently did not lead to an increase in the number of genes in the genome.

We also saw that E. muscae and friends have homologues for the white-collar 1 gene that serves as a blue-light photoreceptor in Neurospora crassa, which may help them with their uncanny timing of behavior manipulation and death.

For those of you who just almost hurt themselves trying to pronounce that genus name, take a deep breath and try this: en-toe-MOP-thor-uh.

Entomophthora muscae is the causative agent of zombie fruit flies! https://youtu.be/C2Jw5ib-s_I?si=0CxYpyLuQGEf8OdA

Yes, zombie fruit flies are a thing! No, this fungus doesn’t infect humans (don’t worry - you definitely weren’t the only person wondering!)

Of course, these fruit flies are not actually reanimated corpses - we call them zombies because they cease being in control of their own behavior - the fungus takes over!

Flies that are infected with E. muscae ultimately die, but right before death the fungus drives them to climb upwards, affix themselves to the substrate and strike an uncanny death pose.

This behavior manipulation aids in spore dispersal, but how these fungi accomplish this—while growing within their fly host—still remains only partly understood (https://elifesciences.org/articles/85410 https://doi.org/10.1038/s41396-022-01284-x)

In our preprint we describe the sequencing, assembly and analysis of the E. muscae genome, revealing a suite of interesting findings about these highly-specialized pathogens, including expansions of proteins that break down insect blood sugar and those that degrade insulin.

I see you thinking to yourself - you sequenced a fungal genome? Big deal! Fungal genomes are small - I can sequence a fungal genome in my sleep.

Oh friend, in this case you are very incorrect. Not only is it challenging to isolate DNA from this group of fungi, but their genomes are some of the largest and most repetitive to date, presenting further challenges for sequencing and assembly.

So how did we do this? A combination of modifying the extraction protocols (http://dx.doi.org/10.17504/protocols.io.rm7vzyje2lx1/v1…) having on-demand access to E. muscae fungal culture and being very, very persistent.

Then we took advantage of long-read sequencing, which, in our puzzle analogy, made the pieces more distinct from each other and therefore easier to put back together.

Finally, we looked at the correspondence between morphology and sequence data in E. muscae species. For a long time, we’ve decided that things are E. muscae based on how they look…but genetic data tells a more complex story.

Tl; dr - it’s time to incorporate sequencing info along with morphology in our identification. The different isolates that we call E. muscae could very well be different species, even!