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Elya, C.

Publications and source records attributed to Elya, C..

5 recordsLinked to original sources

Evidence that Entomophthora muscae controls the timing of host death via its own circadian clock

Timing in the natural world is a matter of life or death; consequently, nearly all life on Earth has evolved internal circadian clocks. Many behavior-manipulating parasites exhibit striking daily timing, but whether this is clock-driven has remained unclear. Here, we leveraged the laboratory-tractable zombie fruit fly model, Drosophila melanogaster infected by the behavior manipulating fungus Entomophthora muscae, to tackle this long standing mystery. Using an automated behavioral paradigm, we found that the timing of death of wild-type flies continues to occur with [~]21 hour periodicity in the absence of environmental cues, indicating that death is controlled by a system-intrinsic clock. Experiments with circadian and photoreception mutants revealed that death is independent of host genotype, suggesting that the host does not drive this rhythm and raising the possibility that timing is dictated by E. muscae. Transcriptomic analysis of in vitro grown fungus revealed that E. muscae maintains rhythmic gene expression independent of the fly host that peaks at sunset and has a free-running period of [~]22 hours. Among cycling genes, we identified a transcript encoding a protein with high homology to white collar-1, the blue light sensor and core component of the molecular oscillator in the model ascomycete fungus Neurospora crassa. Altogether, our findings suggest that E. muscae has an endogenous circadian clock. Given that the host genetic background does not appear to dictate the timing of death, our results suggest that the E. muscae clock may be the primary driver of this rhythm. Our work supports a model in which a fungal clock influences fly outcomes, suggesting that endogenous parasitic clocks may play a broader role in the temporal coordination of host manipulation.

microbiology↗

Signatures of transposon-mediated genome inflation, host specialization, and photoentrainment in Entomophthora muscae and allied entomophthoralean fungi

Despite over a century of observations, the obligate insect parasites within the order Entomophthorales remain poorly characterized at the genetic level. This is in part due to their large genome sizes and difficulty in obtaining sequenceable material. In this manuscript, we leveraged a recently-isolated, laboratory-tractable Entomophthora muscae isolate and improved long-read sequencing to obtain a largely-complete entomophthoralean genome. Our E. muscae assembly is 1.03 Gb, consists of 7,810 contigs and contains 81.3% complete fungal BUSCOs. Using a comparative approach with other available (transcriptomic and genomic) datasets from entomophthoralean fungi, we provide new insight into the biology of these understudied pathogens. We offer a head-to-head comparison of morphological and molecular data for species within the E. muscae species complex. Our findings suggest that substantial taxonomic revision is needed to define species within this group and we provide recommendations for differentiating strains and species in the context of the existing body of E. muscae scientific literature. We show that giant genomes are the norm within Entomophthoraceae owing to extensive, but not recent, Ty3 retrotransposon activity, despite the presence of machinery to defend against transposable elements(RNAi). In addition, we find that E. muscae and its closest allies are enriched for M16A peptidases and possess genes that are likely homologs to the blue-light sensor white-collar 1, a Neurospora crassa gene that has a well-established role in maintaining circadian rhythms. We find that E. muscae has an expanded group of acid-trehalases, consistent with trehalose being the primary sugar component of fly (and insect) hemolymph. We uncover evidence that E. muscae diverged from other entomophthoralean fungi by expansion of existing families, rather than loss of particular domains, and possesses a potentially unique suite of secreted catabolic enzymes, consistent with E. muscaes species-specific, biotrophic lifestyle. Altogether, we provide a genetic and molecular foundation that we hope will provide a platform for the continued study of the unique biology of entomophthoralean fungi.

genomics↗

Neural mechanisms of parasite-induced summiting behavior in 'zombie' Drosophila

For at least two centuries, scientists have been enthralled by the "zombie" behaviors induced by mind-controlling parasites. Despite this interest, the mechanistic bases of these uncanny processes have remained mostly a mystery. Here, we leverage the recently established Entomophthora muscae-Drosophila melanogaster "zombie fly" system to reveal the molecular and cellular underpinnings of summit disease, a manipulated behavior evoked by many fungal parasites. Using a new, high-throughput behavior assay to measure summiting, we discovered that summiting behavior is characterized by a burst of locomotion and requires the host circadian and neurosecretory systems, specifically DN1p circadian neurons, pars intercerebralis to corpora allata projecting (PI-CA) neurons and corpora allata (CA), who are solely responsible for juvenile hormone (JH) synthesis and release. Summiting is a fleeting phenomenon, posing a challenge for physiological and biochemical experiments requiring tissue from summiting flies. We addressed this with a machine learning classifier to identify summiting animals in real time. PI-CA neurons and CA appear to be intact in summiting animals, despite E. muscae cells invading the host brain, particularly in the superior medial protocerebrum (SMP), the neuropil that contains DN1p axons and PI-CA dendrites. The blood-brain barrier of flies late in their infection was significantly permeabilized, suggesting that factors in the hemolymph may have greater access to the central nervous system during summiting. Metabolomic analysis of hemolymph from summiting flies revealed differential abundance of several compounds compared to non-summiting flies. Transfusing the hemolymph of summiting flies into non-summiting recipients induced a burst of locomotion, demonstrating that factor(s) in the hemolymph likely cause summiting behavior. Altogether, our work reveals a neuro-mechanistic model for summiting wherein fungal cells perturb the flys hemolymph, activating the neurohormonal pathway linking clock neurons to juvenile hormone production in the CA, ultimately inducing locomotor activity in their host.

neuroscience↗

A fungal pathogen that robustly manipulates the behavior of Drosophila melanogaster in the laboratory

Many microbes induce striking behavioral changes in their animal hosts, but how they achieve this is poorly understood, especially at the molecular level. Mechanistic understanding has been largely constrained by the lack of a model system with advanced tools for molecular manipulation. We recently discovered a strain of the behavior-manipulating fungal pathogen Entomophthora muscae infecting wild Drosophila, and established methods to infect D. melanogaster in the lab. Lab-infected flies manifest the moribund behaviors characteristic of E. muscae infection: hours before death, they climb upward, extend their proboscides and affix in place, then raise their wings, clearing a path for infectious spores to launch from their abdomens. We found that E. muscae invades the fly nervous system, suggesting a direct means by which the fungus could induce behavioral changes. Given the vast molecular toolkit available for D. melanogaster, we believe this new system will enable rapid progress in understanding the mechanistic basis of E. muscaes behavioral manipulation in the fly.

animal behavior and cognition↗

Or22 allelic variation alone does not explain differences in discrimination of yeast-produced volatiles by D. melanogaster

Different lines of the fruit fly Drosophila melanogaster show variation in the ability to discriminate between volatiles produced by the yeast Saccharomyces cerevisiae under natural (nitrogen-limiting, YVN) or laboratory (sugar-limiting, YVL) conditions. Previous work in our laboratory uncovered a strong correlation between heightened sensitivity to YVN wild D. melanogaster lines that harbored a chimeric variant of the highly variable odorant receptor 22 (Or22) locus of D. melanogaster. We sought to determine if this trend held for an extended set of D. melanogaster lines, if observed variation within chimeric and non-chimeric lines could be explained by nucleotide polymorphisms and if replacing Or22 with a chimeric allele in a non-chimeric background could confer the enhanced ability to detect YVN. In parallel, we performed crosses of chimeric and non-chimeric fly lines and assayed the behavior of their progeny for enhanced sensitivity to YVN to assess the heritability of the Or22 locus. Ultimately, we found that, while the overall trend of increased sensitivity to YVN in chimeric lines persists, there are exceptions and variation that cannot be explained by sequence variation at the Or22 locus. In addition, we did not observe increased sensitivity for YVN upon replacing the Or22 allele in a non-chimeric line (OreR) with that from our most YVN-sensitive, chimeric line (ME). Though our results do not support our hypothesis that Or22 is the primary driver of sensitivity to YVN, Or22 remains an interesting locus in the context of fly-yeast ecology.

genetics↗