Drosophila melanogaster | EPFL Graph Search

Drosophila melanogaster is a species of fly (the taxonomic order Diptera) in the family Drosophilidae. The species is often referred to as the fruit fly or lesser fruit fly, or less commonly the "vinegar fly" or "pomace fly". Starting with Charles W. Woodworth's 1901 proposal of the use of this species as a model organism, D. melanogaster continues to be widely used for biological research in genetics, physiology, microbial pathogenesis, and life history evolution. As of 2017, six Nobel Prizes have been awarded to drosophilists for their work using the insect. D. melanogaster is typically used in research owing to its rapid life cycle, relatively simple genetics with only four pairs of chromosomes, and large number of offspring per generation. It was originally an African species, with all non-African lineages having a common origin. Its geographic range includes all continents, including islands. D. melanogaster is a common pest in homes, restaurants, and other places where food is s

The nuclear cofactor DOR regulates autophagy in mammalian and Drosophila cells

Jordi Duran

The regulation of autophagy in metazoans is only partly understood, and there is a need to identify the proteins that control this process. The diabetes- and obesity-regulated gene (DOR), a recently reported nuclear cofactor of thyroid hormone receptors, is expressed abundantly in metabolically active tissues such as muscle. Here, we show that DOR shuttles between the nucleus and the cytoplasm, depending on cellular stress conditions, and re-localizes to autophagosomes on autophagy activation. We demonstrate that DOR interacts physically with autophagic proteins Golgi-associated ATPase enhancer of 16 kDa (GATE16) and microtubule-associated protein 1A/1B-light chain 3. Gain-of-function and loss-of-function studies indicate that DOR stimulates autophagosome formation and accelerates the degradation of stable proteins. CG11347, the DOR Drosophila homologue, has been predicted to interact with the Drosophila Atg8 homologues, which suggests functional conservation in autophagy. Flies lacking CG11347 show reduced autophagy in the fat body during pupal development. All together, our data indicate that DOR regulates autophagosome formation and protein degradation in mammalian and Drosophila cells.

2009

The double-edged toxins

Mario Gonzalo Garcia Arraez

Many insect species are associated with endosymbiotic bacteria which have the particularity of living within host tissues. Endosymbionts benefit from this stable and nutritious environment, while providing ecological advantages to their host, such as protection against parasites or thermal tolerance. Spiroplasma poulsonii is an endosymbiotic bacterium that infects natural populations of Drosophila melanogaster. Spiroplasma poulsonii lacks a cell wall, a fact that renders it invisible to the host immune system and allows it to thrive in the host hemolymph. It invades the female germline by co-opting the hostâs yolk transport and uptake machinery, which ensures its vertical transmission. Its efficient transmission is associated with a phenotype called male-killing, whereby infected male embryos die during their early development while infected females survive. The mechanisms that ensure the stability of Drosophila-Spiroplasma symbiosis are increasingly well understood, but the bacterial genes involved remain poorly known because of the intractability of Spiroplasma. This project aims at better characterizing the Drosophila-Spiroplasma interaction, with particular focus on the bacterial side. In the first part, I developed a method to cultivate Spiroplasma poulsonii in vitro by optimizing a commercially available medium. This culture method allowed comparing the transcriptome of in vitro grown versus host-grown Spiroplasma, enabling us to identify putative genes involved in the interaction with the host. Interestingly, inside its insect host, S. poulsonii up-regulates genes coding for toxins of the Ribosomal Inactivating Protein (RIP) family. RIPs were previously known for their role in host protection against macro-parasites, such as wasps and nematodes. Their up-regulation in unparasitized hosts compared to culture was thus peculiar, raising the question what effect these RIPs have on host biology. Thus, in the second part, I studied the function of S. poulsonii RIPs in the absence of parasites. I showed that two of them are constantly expressed within the host and provide evidence that these toxins shorten host life span and increase embryonic mortality. Interestingly, the expression of RIPs was more toxic to male embryos than females, suggesting that RIPs contribute to S. poulsonii-induced male-killing. Last, I studied the D. melanogaster response to RIPs, and how the host mitigates the deleterious effects of these toxins by up-regulating the cytosolic chaperone Heat-Shock-Protein 70B (HSP70B). This protein carries out essential functions in protein homeostasis under normal and stressful conditions such as folding, refolding, or increasing the half-life of proteins. Interestingly, up-regulation of Hsp70B in the presence of RIPs results in an increased lifespan and in a better tolerance to heat stress, which may be ecologically advantageous. Altogether, this work illustrates how Spiroplasma-derived RIP toxins can differentially affect Drosophila depending on the ecological context, ranging from beneficial upon parasite infection or heat shock to detrimental in the absence of such environmental pressures.

EPFL2018

The role of immune effectors in controlling Drosophila-microbes interactions

Alice Marra

All live beings are in constant interaction with microorganisms that may be beneficial, deleterious or commensal. Insects in particular live in close contact with microorganisms. This is especially true for species, like the fruit fly Drosophila melanogaster that feed, lay eggs and develop on or close to decomposing organic matter. In contrast to vertebrates, insects did not evolve an adaptive immune system to combat pathogens selectively. They instead rely on surprisingly efficient innate defense mechanisms for the control and clearance of all microbes without any species-specific targeting. Innate immunity encompasses a wide range of mechanisms that rely on direct pathogen recognition and elimination. In addition, metabolic and behavioral responses also strongly affect the outcome of insect interactions with both pathogenic and non-pathogenic bacteria. Although the Drosophila immune system has been extensively described, little is known about the role of immune effectors in tolerating and controlling symbiotic microbes. For this reason, during my PhD studies, I investigated how Drosophila melanogaster immune effectors differentially interact with mutualistic symbionts. First, I investigated the role of some of the host antimicrobials, called antimicrobial peptides and lysozymes, in maintaining the homeostasis of the gut microbiota. I found that both antimicrobial peptides and lysozymes can actively regulate the gut microbiota composition and abundancy, especially during aging. In a second part of my thesis, I got interested in Spiroplasma, a heritable symbiotic bacterium that lives within the fly hemolymph. I characterized the role of the Drosophila iron transporter Transferrin 1 (Tsf1) during Spiroplasma-Drosophila symbiosis. I first showed that mutant flies for tsf1 have an impaired Spiroplasma load, due to iron relocation from the hemolymph to the fat body, where it becomes inaccessible for Spiroplasma. Furthermore, I demonstrated that Spiroplasma scavenges host iron only when it is bound to the protein, which points to Tsf1 and iron transport as a control mechanism for hemolymphatic symbionts. Collectively, my studies contribute to a better understanding of how the innate immune effectors interact with Drosophila microbial symbionts to both regulate and maintain stable, long-lasting, interactions.

EPFL2021