Background: Subdued is a calcium-activated chloride channel of the anoctamin family in Drosophila. Results: Knockout or knockdown of subdued leads to defective nociceptive responses to heat. Conclusion: The Subdued channel mediates thermal nociception. Significance: An anoctamin channel participates in thermal nociception in insects.
The Drosophila drop-dead (drd) mutant undergoes massive brain degeneration, resulting in sudden death. drd encodes a multi-pass membrane protein possessing nose resistant to fluoxetine (NRF) and putative acyltransferase domains. However, the etiology of brain degeneration that occurs in drd mutant flies is still poorly understood. Herein, we show that drd neurodegeneration may be because of an oxygen deficit in the brain. We found that DRD protein is selectively expressed in cells secreting cuticular and eggshell layers. These layers exhibit blue fluorescence upon UV excitation, which is reduced in drd flies. The drd tracheal air sacs lacking blue fluorescence collapse, which likely contributes to hypoxia. Consistently, genes induced in hypoxia are up-regulated in drd flies. Feeding of anti-reactive oxygen species agents partially rescue the drd from sudden death. We propose that drd flies can provide a noninvasive animal model for hypoxia-induced cell death.
Age-related decline in stem cell function is observed in many tissues from invertebrates to humans. While cell intrinsic alterations impair stem cells, aging of the stem cell niche also significantly contributes to the loss of tissue homeostasis associated with reduced regenerative capacity. Hub cells, which constitute the stem cell niche in the
Drosophila
testis, exhibit age-associated decline in number and activities, yet underlying mechanisms are not fully understood. Here we show that Lin28, a highly conserved RNA binding protein, is expressed in hub cells and its expression dramatically declines in old testis.
lin28
mutant testes exhibit hub cell loss and defective hub architecture, recapitulating the normal aging process. Importantly, maintained expression of Lin28 prolongs hub integrity and function in aged testes, suggesting that Lin28 decline is a driver of hub cell aging. Mechanistically, the level of unpaired (
upd)
, a stem cell self-renewal factor, is reduced in
lin28
mutant testis and Lin28 protein directly binds and stabilizes
upd
transcripts, in a let-7 independent manner. Altogether, our results suggest that Lin28 acts to protect
upd
transcripts in hub cells, and reduction of Lin28 in old testis leads to decreased
upd
levels, hub cell aging and loss of the stem cell niche.
The mechanosensory neurons of Drosophila larvae are demonstrably activated by diverse mechanical stimuli, but the mechanisms underlying this function are not completely understood. Here we report a genetic, immunohistochemical, and electrophysiological analysis of the Ppk30 ion channel, a member of the Drosophila pickpocket (ppk) family, counterpart of the mammalian Degenerin/Epithelial Na+ Channel family. Ppk30 mutant larvae displayed deficits in proprioceptive movement and mechanical nociception, which are detected by class IV sensory (mdIV) neurons. The same neurons also detect heat nociception, which was not impaired in ppk30 mutant larvae. Similarly, Ppk30 mutation did not alter gentle touch mechanosensation, a distinct mechanosensation detected by other neurons, suggesting that Ppk30 has a functional role in mechanosensation in mdIV neurons. Consistently, Ppk30 was expressed in class IV neurons, but was not detectable in other larval skin sensory neurons. Mutant phenotypes were rescued by expressing Ppk30 in mdIV neurons. Electrophysiological analysis of heterologous cells expressing Ppk30 did not detect mechanosensitive channel activities, but did detect acid‐induced currents. These data show that Ppk30 has a role in mechanosensation, but not in thermosensation, in class IV neurons, and possibly has other functions related to acid response.
The germline stem cells of the Drosophila ovary continuously
produce eggs throughout the life- span. Intricate regulation of stemness and
differentiation is critical to this continuous production. The translational
regulator Nos is an intrinsic factor that is required for maintenance of
stemness in germline stem cells. Nos expression is reduced in differentiating
cells at the post-transcriptional level by diverse translational regulators.
However, molecular mechanisms underlying Nos repression are not completely
understood. Through three distinct protein-protein interaction experiments, we
identified specific molecular interactions between translational regulators
involved in Nos repression. Our findings suggest a model in which protein
complexes assemble on the 3’ untranslated region of Nos mRNA in order to
regulate Nos expression at the post-transcriptional level.
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