Cellular and molecular organization of the
            <i>Drosophila</i>
            foregut

Zhu, Haolong; Ludington, William B.; Spradling, Allan C.

doi:10.1073/pnas.2318760121

Cited by 7 publications

References 81 publications

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The intestinal stem cell/enteroblast-GAL4 driver, escargot-GAL4, also manipulates gene expression in the juvenile hormone-synthesizing organ of Drosophila melanogaster

Kurogi,

Mizuno,

Kamiyama

et al. 2024

Sci Rep

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Intestinal stem cells (ISCs) of the fruit fly, Drosophila melanogaster, offer an excellent genetic model to explore homeostatic roles of ISCs in animal physiology. Among available genetic tools, the escargot (esg)-GAL4 driver, expressing the yeast transcription factor gene, GAL4, under control of the esg gene promoter, has contributed significantly to ISC studies. This driver facilitates activation of genes of interest in proximity to a GAL4-binding element, Upstream Activating Sequence, in ISCs and progenitor enteroblasts (EBs). While esg-GAL4 has been considered an ISC/EB-specific driver, recent studies have shown that esg-GAL4 is also active in other tissues, such as neurons and ovaries. Therefore, the ISC/EB specificity of esg-GAL4 is questionable. In this study, we reveal esg-GAL4 expression in the corpus allatum (CA), responsible for juvenile hormone (JH) production. When driving the oncogenic gene, RasV12, esg-GAL4 induces overgrowth in ISCs/EBs as reported, but also increases CA cell number and size. Consistent with this observation, animals alter expression of JH-response genes. Our data show that esg-GAL4-driven gene manipulation can systemically influence JH-mediated animal physiology, arguing for cautious use of esg-GAL4 as a “specific” ISC/EB driver to examine ISC/EB-mediated animal physiology.

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The intestinal stem cell/enteroblast-GAL4 driver, escargot-GAL4, also manipulates gene expression in the juvenile hormone-synthesizing organ of Drosophila melanogaster

Kurogi,

Mizuno,

Kamiyama

et al. 2024

Sci Rep

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Humidity determines penetrance of a latitudinal gradient in genetic selection on the microbiota byDrosophila melanogaster

Massey,

Nosker,

Gale

et al. 2024

Preprint

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The fruit fly Drosophila melanogaster is a model for understanding how hosts and their microbial partners interact as the host adapts to wild environments. These interactions are readily interrogated because of the low taxonomic and numeric complexity of the flies' bacterial communities. Previous work has established that host genotype, the environment, diet, and interspecies microbial interactions can all influence host fitness and microbiota composition, but the specific processes and characters mediating these processes are incompletely understood. Here, we compared the variation in microbiota composition between wild-derived fly populations when flies could choose between the microorganisms in their diets and when flies were reared under environmental perturbation (different humidities). We also compared the colonization of the resident and transient microorganisms. We show that the ability to choose between microorganisms in the diet and the environmental condition of the flies can influence the relative abundance of the microbiota. There were also key differences in the abundances of the resident and transient microbiota. However, the microbiota only differed between populations when the flies were reared at humidities at or above 50% relative humidity. We also show that elevated humidity determined the penetrance of a gradient in host genetic selection on the microbiota that is associated with the latitude the flies were collected from. Finally, we show that the treatment-dependent variation in microbiota composition is associated with variation in host stress survival. Together, these findings emphasize that host genetic selection on the microbiota composition of a model animal host can be patterned with the source geography, and that such variation has the potential to influence their survival in the wild.

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Selective autophagy fine-tunes Stat92E activity by degrading Su(var)2-10/PIAS during glial injury signaling inDrosophila

Vincze,

Esküdt,

Fehér-Juhász

et al. 2024

Preprint

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Glial immunity plays a pivotal role in the maintenance of nervous system homeostasis and in responses to stress conditions, including neural injuries. The transcription factor Stat92E is activated independently of the canonical JAK/STAT pathway inDrosophilaglial cells following central nervous system injury to shape glial reactivity towards degenerating axons. However, the upstream regulatory mechanisms governing Stat92E activation remain elusive. Here we reveal that selective autophagy mediates degradation of the PIAS SUMO ligase family member Stat92E repressor, Su(var)2-10 in glia. Autophagic elimination of Su(var)2-10 mediated by its co-localization and interaction with the core autophagy factor Atg8a is required for efficient Stat92E-dependent transcription after injury. In line with this, we demonstrate that autophagy is essential for the upregulation of an innate immune pathway in glial cells following axon injury, characterized by the induction ofvirus-induced RNA 1(vir-1). We propose that autophagic Su(var)2-10 breakdown controls Stat92E activation to allow glial reactivity. These findings identify a critical role for autophagy in glial immunity as part of neural injury responses.

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Cellular and molecular organization of the Drosophila foregut

Cited by 7 publications

References 81 publications

The intestinal stem cell/enteroblast-GAL4 driver, escargot-GAL4, also manipulates gene expression in the juvenile hormone-synthesizing organ of Drosophila melanogaster

The intestinal stem cell/enteroblast-GAL4 driver, escargot-GAL4, also manipulates gene expression in the juvenile hormone-synthesizing organ of Drosophila melanogaster

Humidity determines penetrance of a latitudinal gradient in genetic selection on the microbiota byDrosophila melanogaster

Selective autophagy fine-tunes Stat92E activity by degrading Su(var)2-10/PIAS during glial injury signaling inDrosophila

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