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Tuesday August 11th - Physiology and Metabolism

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De Donno, M. D., Mercuri, E., Balena, B., Zangaro, F., Bozzetti, M. P., Specchia, V. (2025). Mechanistic insights into cadmium-related premature aging in Drosophila model. Front Neurosci, 19:1605687 PubMed ID: 40535972
Summary:
The intricate and multifaceted relationship between environmental pollutants, particularly heavy metals such as cadmium, and human health has been extensively documented, with a significant focus on their neurotoxic effects. Notably, the connection between cadmium exposure and Alzheimer's disease is becoming increasingly evident, prompting a deeper investigation into the underlying mechanisms at play. Despite the growing body of evidence linking cadmium to neurodegeneration and although harmful molecular activities of cadmium in cells have been demonstrated, the precise molecular mechanism induced by this toxic metal within neuronal cells remains largely enigmatic. This study aims to shed light on these mechanistic processes by utilizing Drosophila melanogaster. Through a carefully designed approach, chronic exposure to cadmium was simulated, which allowed observation of the resulting effects on the flies over time. The findings revealed that chronic cadmium exposure led to premature aging in flies, characterized by neurodegeneration and an exacerbation of complex neurological phenotypes. Notably, these included significant impairments in learning and memory, which are critical cognitive functions often compromised in neurodegenerative conditions. With the aim of exploring the mechanistic underpinnings of these observations, this s determined that cadmium impairs RNP formation and could disrupt the delicate process of liquid-liquid phase separation within neuronal cells. This disruption appears to play a pivotal role in initiating the cascade of events that contribute to neurodegeneration. Liquid-liquid phase separation is essential for the proper organization of cellular components and the maintenance of neuronal health; thus, cadmium's interference in this process may provide a crucial insight into its neurotoxic effects.
Di Dio, C., Porrazzo, A., De Gregorio, A., Morciano, P., Tabocchini, M. A., Cenci, G., Cipressa, F., Esposito, G. (2025). TIn vivo study of the radioadaptive response and low-dose hyper-radiosensitivity for chromosome breaks induced by gamma rays in wild-type Drosophila melanogaster larval neuroblasts: Dose and dose rate dependence. PLoS One, 20(6):e0325608 PubMed ID: 40489495
Summary:
Although the biological effects of low doses/dose rates of ionising radiation have been extensively studied both in vitro and in vivo, there are still knowledge gaps to be filled. For example, the mechanisms underlying the phenomena of radioadaptive responses and hypersensitivity to low doses of radiation are still not fully understood. This study aims to investigate the phenomenon of radioadaptive response in Drosophila melanogaster larval neuroblasts, focusing on the influence of different gamma priming doses and priming dose rates. This study examined the modulation of cytogenetic damage, specifically the frequency of chromosome breaks, induced by a challenging dose of 10 Gy following different priming doses (0-2.7 Gy) delivered at dose rates ranging from 1.4 to 17 mGy/h. The findings reveal the presence of a distinct window in which radioadaptive responses occurs, notably above a certain threshold dose when delivered at a rate of 1.4 mGy/h. Consistently with previous results, this study confirmed that the maximal protection was observed at a priming dose of 0.4 Gy delivered at 2.5 mGy/h. Additionally, the occurrence of chromosome breaks was studied after irradiating larval neuroblasts at doses ranging from 0.7 to 10 Gy. Notably, in this case a low-dose hyper-radiosensitivity phenomenon was observed up to 2.7 Gy, followed by increased resistance above 2.7 Gy. These results provide insight into the complex cellular responses to low-dose/dose rate radiation and have implications in various fields, including radiation protection, diagnostics, theragnostics and biodosimetry.
Bhattacharya, D., Abaquita, T. L. A., Gorska-Andrzejak, J., Pyza, E. (2025). The Influence of Caffeine on Siesta and Nighttime Sleep in Drosophila melanogaster. Dev Neurobiol, 85(3):e22987 PubMed ID: 40525487
Summary:
Caffeine, a plant-derived psychostimulant, has been demonstrated to reduce sleep and increase dopaminergic neuron activity in mammals through competitive antagonism at adenosine receptors (AdoRs). However, the extent to which it influences daytime sleep (siesta) as much as nighttime sleep and the involvement of the adenosine signaling pathway in this process remain unsolved. It is similarly unclear whether the influence of caffeine varies with age and depends on sex and what type of cells it affects most; the clock cells that are involved in sleep timing and regulation or dopaminergic neurons, which are crucial for voluntary movement. To address this question, the role of caffeine has been investigated in Drosophila melanogaster (wild-type Canton-S flies), which has also been observed to reduce sleep in response to caffeine. The siesta and nighttime sleep of 3-, 30-, and 50-day-old males and females of Canton-S Drosophila were examined. Furthermore, transgenic flies with overexpressed or silenced dAdoR in all neurons (elav-expressing cells), the circadian clock cells (tim-expressing cells), and dopaminergic neurons (th-expressing cells) were studied. Females exhibited greater sensitivity to caffeine than males, and older flies slept longer during the day than young flies. However, caffeine treatment resulted in reducing siesta in flies with overexpression of dAdoR in all neurons, tim-, and th-expressing cells. Conversely, silencing of dAdoR increased siesta. Therefore, the observed differences in the daytime sleep of Drosophila appeared to depend on signaling through AdoRs.
Wang, R., Zhu, Q., Huang, H., Yang, M., Wang, X., Dong, Y., Li, Y., Guan, Y., Zhong, L., Niu, Y. (2024). Periodic protein-restricted diets extend the lifespan of high-fat diet-induced Drosophila melanogaster males. Aging Cell:e14327 PubMed ID: 39207121
Summary:
Research has shown that sustained protein restriction can improve the effects of a high-fat diet on health and extend lifespan. However, long-term adherence to a protein-restricted diet is challenging. Therefore, this study used a fly model to investigate whether periodic protein restriction (PPR) could also mitigate the potential adverse effects of a high-fat diet and extend healthy lifespan. This study's results showed that PPR reduced body weight, lipid levels, and oxidative stress induced by a high-fat diet in flies and significantly extended the healthy lifespan of male flies. Lipid metabolism and transcriptome results revealed that the common differences between the PPR group and the control group and high-fat group showed a significant decrease in palmitic acid in the PPR group; the enriched common differential pathways Toll and Imd were significantly inhibited in the PPR group. Further analysis indicated a significant positive correlation between palmitic acid levels and gene expression in the Toll and Imd pathways. This suggests that PPR effectively improves fruit fly lipid metabolism, reduces palmitic acid levels, and thereby suppresses the Toll and Imd pathways to extend the healthy lifespan of flies. This study provides a theoretical basis for the long-term effects of PPR on health and offers a new dietary adjustment option for maintaining health in the long term.
Deng, X., Wang, W., Peng, D., Zhang, L., Ma, Z., Fu, J., Tong, C., Xu, Y. (2025). Optogenetic perturbation of lipid droplet localization affects lipid metabolism and development in Drosophila. J Lipid Res:100848 PubMed ID: 40545239
Summary:
Lipid droplets (LDs) are dynamic organelles crucial for lipid storage and homeostasis. Despite extensive documentation of their importance, the causal relationship between LD localization and function in health and disease remains inadequately understood. This study developed optogenetics-based tools, termed 'Opto-LDs', which facilitate the interaction between LDs and motor proteins in a light-dependent manner, enabling precise control of LD localization within cells. Utilizing these optogenetic modules, this study demonstrated that light-induced relocation of LDs to the periphery of hepatocytes results in elevated very-low-density lipoprotein (VLDL) secretion, recapturing the beneficial effect of insulin in vitro. Furthermore, studies in transgenic Drosophila revealed that proper LD localization is critical for embryonic development, with mistargeting of LDs significantly affecting egg success of hatching into first instar larvae. In summary, this work underscores the great importance of LD localization in lipid metabolism and development, and the developed tools offer valuable insights into the functions of LDs in health and disease.
Boumard, B., Le Meur, G., Aboutine, L., Stefanutti, M., Maalouf, T., El-Hajj, M., Choi, B. J., Bauer, R., Bardin, A. J. (2025). Cell-type-specific nucleotide sharing through gap junctions impacts sensitivity to replication stress in Drosophila. Dev Cell, PubMed ID: 40480229
Summary:
Cell proliferation, which underlies tissue growth and homeostasis, requires high levels of metabolites such as deoxynucleotides (dNTPs). The dNTP pool is known to be tightly and cell-autonomously regulated via de novo synthesis and salvage pathways. Tis study demonstrated that nucleotides can also be provided to cells non-autonomously by surrounding cells within a tissue. Using Drosophila epithelial tissues as models, this study found that adult intestinal stem cells (ISCs) are highly sensitive to nucleotide depletion, whereas wing progenitor cells are not. Wing progenitor cells share nucleotides through gap junction connections, allowing buffering of replication stress induced by nucleotide pool depletion. Adult ISCs, however, lack gap junctions and cannot receive dNTPs from neighbors. Collectively, these data suggest that gap-junction-dependent sharing between cells can contribute to dNTP pool homeostasis in vivo. It is proposed that inherent differences in cellular gap junction permeability can influence sensitivity to fluctuations in intracellular dNTP levels.
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Thursday August 7th - Adult Development

Li, J., Ning, C., Liu, Y., Deng, B., Wang, B., Shi, K., Wang, R., Fang, R., Zhou, C. (2024). The function of juvenile-adult transition axis in female sexual receptivity of Drosophila melanogaster. Elife, 12 PubMed ID: 39240259
Summary:
Female sexual receptivity is essential for reproduction of a species. Neuropeptides play the main role in regulating female receptivity. However, whether neuropeptides regulate female sexual receptivity during the neurodevelopment is unknown. This study found the peptide hormone prothoracicotropic hormone (A hrefPTTH), which belongs to the insect PG (prothoracic gland) axis, negatively regulated virgin female receptivity through ecdysone during neurodevelopment in Drosophila melanogaster. This study identified PTTH neurons as doublesex-positive neurons, they regulated virgin female receptivity before the metamorphosis during the third-instar larval stage. PTTH deletion resulted in the increased EcR-A expression in the whole newly formed prepupae. Furthermore, the ecdysone receptor EcR-A in pC1 neurons positively regulated virgin female receptivity during metamorphosis. The decreased EcR-A in pC1 neurons induced abnormal morphological development of pC1 neurons without changing neural activity. Among all subtypes of pC1 neurons, the function of EcR-A in pC1b neurons was necessary for virgin female copulation rate (for information on pC1b neurons, go to Google and enter pC1b neurons Drosophila). These suggested that the changes of synaptic connections between pC1b and other neurons decreased female copulation rate. Moreover, female receptivity significantly decreased when the expression of PTTH receptor Torso was reduced in pC1 neurons. This suggested that PTTH not only regulates female receptivity through ecdysone but also through affecting female receptivity associated neurons directly. The PG axis has similar functional strategy as the hypothalamic-pituitary-gonadal axis in mammals to trigger the juvenile-adult transition. This work suggests a general mechanism underlying which the neurodevelopment during maturation regulates female sexual receptivity.
Aldrich, J. C., Vanderlinden, L. A., Jacobsen, T. L., Wood, C., Saba, L. M., Britt, S. G. (2024). Genome-Wide Association Study and transcriptome analysis reveals a complex gene network that regulates opsin gene expression and cell fate determination in Drosophila R7 photoreceptor cells. bioRxiv, PubMed ID: 39149333
Summary:
An animal's ability to discriminate between differing wavelengths of light (i.e., color vision) is mediated, in part, by a subset of photoreceptor cells that express opsins with distinct absorption spectra. In Drosophila R7 photoreceptors, expression of the rhodopsin molecules, Rh3 or Rh4, is determined by a stochastic process mediated by the transcription factor Spineless. The goal of this study was to identify additional factors that regulate R7 cell fate and opsin choice using a Genome Wide Association Study (GWAS) paired with transcriptome analysis via RNA-Seq. Rh3 and Rh4 expression was examined in a subset of fully-sequenced inbred strains from the Drosophila Genetic Reference Panel,performed, and a GWAS was performed to identify 42 naturally-occurring polymorphisms-in proximity to 28 candidate genes-that significantly influence R7 opsin expression. Network analysis revealed multiple potential interactions between the associated candidate genes, spineless and its partners. GWAS candidates were further validated in a secondary RNAi screen which identified 12 lines that significantly reduce the proportion of Rh3 expressing R7 photoreceptors. Finally, using RNA-Seq, all but four of the GWAS candidates were demonstrated to be expressed in the pupal retina at a critical developmental time point and that five are among the 917 differentially expressed genes in sevenless mutants, which lack R7 cells. Collectively, these results suggest that the relatively simple, binary cell fate decision underlying R7 opsin expression is modulated by a larger, more complex network of regulatory factors. Of particular interest are a subset of candidate genes with previously characterized neuronal functions including neurogenesis, neurodegeneration, photoreceptor development, axon growth and guidance, synaptogenesis, and synaptic function.
Ramesh, N. A., Box, A. M., Buttitta, L. A. (2024). Post-eclosion growth in the Drosophila Ejaculatory Duct is driven by Juvenile Hormone signaling and is essential for male fertility. bioRxiv, PubMed ID: 39185157
Summary:
The Drosophila Ejaculatory duct (ED) is a secretory tissue of the somatic male reproductive system. The ED is involved in the secretion of seminal fluid components and ED-specific antimicrobial peptides that aid in fertility and the female post-mating response. The ED is composed of secretory epithelial cells surrounded by a layer of innervated contractile muscle. The ED grows in young adult males during the first 24h post-eclosion, but the cell cycle status of the ED secretory cells and the role of post-eclosion ED growth have been unexplored. This study showed that secretory cells of the adult Drosophila ED undergo variant cell cycles lacking mitosis called the endocycle, that lead to an increase in the cell and organ size of the ED post eclosion. The cells largely exit the endocycle by day 3 of adulthood, when the growth of the ED ceases, resulting in a tissue containing cells of ploidies ranging from 8C-32C. The size of the ED directly correlates with the ploidy of the secretory cells, with additional ectopic endocycles increasing organ size. When endoreplication is compromised in ED secretory cells, it leads to reduced organ size, reduced protein synthesis and compromised fertility. Evidence is provided that the growth and endocycling in the young adult male ED is dependent on Juvenile hormone (JH) signaling, and hormone-induced early adult endocycling is suggested to be required for optimal fertility and function of the ED tissue. Use of the ED as a post-mitotic tissue model to study the role of polyploidy in regulating secretory tissue growth and function is proposed.
Zhang, F., Luo, W., Liu, S., Zhao, L., Su, Y. (2024). Protein phosphatase 2A regulates blood cell proliferation and differentiation in Drosophila larval lymph glands. Febs j, PubMed ID: 39185698
Summary:
Protein phosphatase 2A (PP2A), one of the most abundant protein phosphatases, has divergent functions in multiple types of cells. Its inactivation has been closely associated with leukemia diseases. However, the physiological function of PP2A for hematopoiesis has been poorly understood in organisms. Drosophila hematopoiesis parallels the vertebrate counterpart in developmental and functional features but involves a much simpler hematopoietic system. Utilizing the Drosophila major larval hematopoietic organ lymph gland, the function of PP2A for hematopoiesis in vivo was studied. By knocking down the expression of Pp2A-29B that encodes the scaffold subunit of the PP2A holoenzyme complex, this study found that PP2A silencing in the differentiating hemocytes resulted in their excessive proliferation. Furthermore, this PP2A inhibition downregulated the expression of Smoothened (Smo), a crucial component in the Hedgehog pathway, and smo overexpression was able to rescue the phenotypes of PP2A depletion, indicating that Smo functions as a downstream effector of PP2A to restrict the hemocyte proliferation. PDGF/VEGF-receptor (Pvr) overexpression also restored the Smo expression and lymph gland morphology of PP2A silencing, suggesting a PP2A-Pvr-Smo axis to regulate lymph gland growth and hemocyte proliferation. Moreover, inhibiting PP2A activity in the blood progenitor cells promoted their differentiation, but which was independent with Smo. Together, these data suggested that PP2A plays a dual role in the Drosophila lymph gland by preserving the progenitor population and restraining the hemocyte proliferation, to properly regulate the hematopoietic process.
Bose, A., Schuster, K., Kodali, C., Sonam, S., Smith-Bolton, R. K. (2025). The pioneer transcription factor Zelda controls the exit from regeneration and restoration of patterning in Drosophila. Sci Adv, 11(23):eads5743 PubMed ID: 40479065
Summary:
Many animals can regenerate tissues after injury. While the initiation of regeneration has been studied extensively, how the damage response ends and normal gene expression returns is unclear. This study found that in Drosophila wing imaginal discs, the pioneer transcription factor Zelda controls the exit from regeneration and return to normal gene expression. Optogenetic inactivation of Zelda during regeneration disrupted patterning, induced cell fate errors, and caused morphological defects yet had no effect on normal wing development. Using Cleavage Under Targets & Release Using Nuclease, this study identified targets of Zelda important for the end of regeneration, including genes that control wing margin and vein specification, compartment identity, and cell adhesion. GAGA factor and Fork head similarly coordinate patterning after regeneration, and chromatin regions bound by Zelda increase in accessibility during regeneration. Thus, Zelda orchestrates the transition from regeneration to normal gene expression, highlighting a fundamental difference between developmental and regeneration patterning in the wing disc.
Campbell, J. B., Shingelton, A. W., Greenlee, K. J., Gray, A. E., Smith, H. C., Callier, V., Lundquist, T., Harrison, J. F. (2024). HIF-signaling in the prothoracic gland regulates growth and development in hypoxia but not normoxia in Drosophila. The Journal of experimental biology, PubMed ID: 39206603
Summary:
The developmental regulation of body size is a fundamental life-history characteristic that in most animals is tied to the transition from juvenile to adult form. In holometabolous insects this transition is ostensibly initiated at the attainment of a critical weight in the final larval instar. It has been hypothesized that the size-sensing mechanism used to determine attainment of critical weight exploits oxygen limitation as a larvae grows beyond the oxygen-delivery capacity of its fixed tracheal system; that is, developmentally-induced cellular hypoxia initiates the synthesis of the molting hormone ecdysone by the prothoracic gland. This hypothesis was in Drosophila by assaying cellular hypoxia throughout the third-larval instar at 21 and 10 kPa O2, using the activity of the HIF-signalling pathway as a measure of hypoxia. While HIF-signalling was elevated at low levels of environmental O2 it did not markedly increase during development at either oxygen level, and was only suppressed by hyperoxia after feeding had ceased. Further, changes in HIF-signalling in the prothoracic gland alone did not alter body size or developmental time in a way that would be expected if cellular hypoxia in the prothoracic gland was part of the critical weight mechanism. These data do show, however, that reduced HIF-signalling in the prothoracic gland decreases survival and retards development at 10 kPa O2, suggesting that prothoracic HIF-signaling is a necessary part of the beneficial plasticity mechanism that controls growth and development in response to low oxygen level.
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Friday August 1st - Gonads

Zhang, R., Shi, P., Xu, S., Ming, Z., Liu, Z., He, Y., Dai, J., Matunis, E., Xu, J., Ma, Q. (2024). Soma-germline communication drives sex maintenance in the Drosophila testis. National science review, 11(8):nwae215 PubMed ID: 39183747
Summary:
In adult gonads, disruption of somatic sexual identity leads to defective gametogenesis and infertility. However, the underlying mechanisms by which somatic signals regulate germline cells to achieve proper gametogenesis remain unclear. In a previous study, the chinmoSex Transformation) (chinmoST) mutant Drosophila testis phenotype was introduced as a valuable model for investigating the mechanisms underlying sex maintenance. In chinmoST testes, depletion of the Janus Kinase-Signal Transducer and Activator of Transcription downstream effector Chinmo from somatic cyst stem cells (CySCs) feminizes somatic cyst cells and arrests germline differentiation. This study usef single-cell RNA sequencing to uncover chinmoST -specific cell populations and their transcriptomic changes during sex transformation. Comparative analysis of intercellular communication networks between wild-type and chinmoST testes revealed disruptions in several soma-germline signaling pathways in chinmoST testes. Notably, the insulin signaling pathway exhibited significant enhancement in germline stem cells (GSCs). Chinmo cleavage under targets and tagmentation (CUT&Tag) assay revealed that Chinmo directly regulates two male sex determination factors, doublesex (dsx) and fruitless (fru), as well as Ecdysone-inducible gene L2 (ImpL2), a negative regulator of the insulin signaling pathway. Further genetic manipulations confirmed that the impaired gametogenesis observed in chinmoST testes was partly contributed by dysregulation of the insulin signaling pathway. In summary, this study demonstrates that somatic sex maintenance promotes normal spermatogenesis through Chinmo-mediated conserved sex determination and the insulin signaling pathway. This work offers new insights into the complex mechanisms of somatic stem cell sex maintenance and soma-germline communication at the single-cell level. Additionally, these discoveries highlight the potential significance of stem cell sex instability as a novel mechanism contributing to testicular tumorigenesis.
Anderson, M. T., Horne-Badovinac, S. (2025). A complex relationship between the architecture of the basement membrane, its mechanical properties, and its ability to shape the Drosophila egg. Matrix Biol, PubMed ID: 40518025
Summary:
Basement membranes (BMs) are planar extracellular matrices that line the basal surfaces of epithelia and are essential components of most organs. During development, BMs can also play instructive roles in shaping the tissues to which they belong, but how they do so is incompletely understood. The Drosophila egg chamber has become a premier system to study this aspect of BM biology due to the ostensible simplicity of the BM's role in morphogenesis. The prevailing model posits that the egg chamber outer layer of epithelial cells creates a symmetric stiffness gradient in the surrounding BM that preferentially channels egg chamber growth along one axis to create the elongated shape of the egg. There is evidence that the stiffening of the BM depends, in part, on a polarized array of fibrils that form within the BM network, and yet the exact role the BM fibrils play in egg chamber elongation has remained unclear. This study used genetic conditions that abrogate fibril formation to different extents to probe the relationship between the BM's fibril content, its mechanical properties, and the shape of the egg. The results of these experiments are consistent with a model in which BM fibrils influence egg shape by directly augmenting the mechanical properties of the BM. However, this study then examined a final genetic condition that does not fit this simple narrative. It is proposed that the role of the BM in conferring final egg shape is more complicated than previously thought and that some approaches used to study this role should be re-evaluated for their efficacy.
Bischoff, M. C., Norton, J. E., Clark, S. E., Peifer, M. (2025). Plexin/Semaphorin antagonism orchestrates collective cell migration and organ sculpting by regulating epithelial-mesenchymal balance. Sci Adv, 11(25):eadu3741 PubMed ID: 40532000
Summary:
Cell behavior emerges from the intracellular distribution of properties such as protrusion, contractility, and adhesion. Thus, characteristic emergent rules of collective migration can arise from cell-cell contacts locally tweaking architecture, orchestrating self-regulation during development, wound healing, and cancer progression. The Drosophila testis-nascent-myotube system allows dissection of contact-dependent migration in vivo at high resolution. This study describes a role for the axon guidance factor Plexin A in collective cell migration: maintaining cell-cell interfaces at a precise point on the mesenchymal-to-epithelial continuum. This is crucial for testis myotubes (muscle cells that migrate from the genital disc onto the developing testes during metamorphosis) to migrate as a continuous sheet, allowing normal sculpting-morphogenesis. Cells must maintain filopodial N-cadherin-based junctions and remain ECM-tethered near cell-cell contacts to spread while collectively moving. These data further suggest Semaphorin 1b is a Plexin A antagonist, fine-tuning activation. This reveals a contact-dependent mechanism to maintain sheet integrity during migration, driving organ morphogenesis. This is relevant for mesenchymal organ sculpting in other migratory contexts such as angiogenesis.
Andreatta, G., Montagnese, S., Costa, R. (2025). Cold-Sensing TRP Channels and Temperature Preference Modulate Ovarian Development in the Model Organism Drosophila melanogaster. Int J Mol Sci, 26(12) PubMed ID: 40565102
Summary:
Temperature is perceived primarily via transient receptor potential (TRP) channels, which are integral to the molecular machinery sensing environmental and cellular signals. Functional evidence of TRP channel involvement in regulating cold-induced developmental/reproductive responses remains scarce. This study shows that mutations affecting cold-sensing TRP channels antagonize the reduction in development induced by low temperatures (reproductive dormancy) in Drosophila melanogaster. More specifically, mutants for brv1, trp, and trpl significantly lowered dormancy levels at 12 °C and exhibited well-developed oocytes characterized by advanced vitellogenesis. Similarly, functional knockouts for norpA, a gene encoding a phospholipase C acting downstream to Trp and Trpl, exhibited a reduced dormancy response, suggesting that Ca(2+) signaling is key to relaying cold-sensing stimuli during dormancy induction and maintenance. Finally, mutants with an altered temperature preference (i.e., exhibiting impaired cold or warm avoidance) differentially responded to the cold, either lowering or increasing dormancy levels. In summary, this phenotypic analysis provides functional evidence of developmental/reproductive modulation by specific cold-sensing TRP channels in Drosophila melanogaster and indicates that temperature preference affects developmental processes.
Martin-Diaz, J., Herrera, S. C. (2024). A stem cell activation state coupling spermatogenesis with social interactions in Drosophila males. Cell Rep, 43(8):114647 PubMed iD: 39153199
Summary:
Reproduction is paramount to animals. For it to be successful, a coordination of social behavior, physiology, and gamete production is necessary. How are social cues perceived and how do they affect physiology and gametogenesis? While females, ranging from insects to mammals, have provided multiple insights about this coordination, its existence remains largely unknown in males. By using the Drosophila male as a model, this study described a phenomenon by which the availability of potential mating partners triggers an activation state on the stem cell populations of the testis, boosting spermatogenesis. Reliance of spermatogenesis on pheromonal communication, even in the absence of mating or other interactions with females was identified. Finally, the interorgan communication signaling network responsible-muscle-secreted tumor necrosis factor alpha (TNF-α)/Eiger and neuronally secreted octopamine trigger, respectively, the Jun N-terminal kinase (JNK) pathway and a change in calcium dynamics in the cyst stem cells. As a consequence, germ line stem cells increase their proliferation.
Miao, Y. H., Dou, W. H., Liu, J., Huang, D. W., Xiao, J. H. (2024). Single-cell transcriptome sequencing reveals that Wolbachia induces gene expression changes in Drosophila ovary cells to favor its own maternal transmission. mBio:e0147324 PubMed ID: 39194189
Summary:
Wolbachia is an obligate endosymbiont that is maternally inherited and widely distributed in arthropods and nematodes. It remains in the mature eggs of female hosts over generations through multiple strategies and manipulates the reproduction system of the host to enhance its spreading efficiency. However, the transmission of Wolbachia within the host's ovaries and its effects on ovarian cells during oogenesis, have not been extensively studied. Single-cell RNA sequencing was used to comparatively analyze cell-typing and gene expression in Drosophila ovaries infected and uninfected with Wolbachia. The findings indicate that Wolbachia significantly affects the transcription of host genes involved in the extracellular matrix, cytoskeleton organization, and cytomembrane mobility in multiple cell types, which may make host ovarian cells more conducive for the transmission of Wolbachia from extracellular to intracellular. Moreover, the genes nos and orb, which are related to the synthesis of ribonucleoprotein complexes, are specifically upregulated in early germline cells of ovaries infected with Wolbachia, revealing that Wolbachia can increase the possibility of its localization to the host oocytes by enhancing the binding with host ribonucleoprotein-complex processing bodies (P-bodies). All these findings provide novel insights into the maternal transmission of Wolbachia between host ovarian cells.
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