Biology subjects

Hafezi, Y.

Publications and source records attributed to Hafezi, Y..

3 recordsLinked to original sources

bioRxiv2026

No detectable effect of P2 neurons on female post-mating changes in sleep and feeding in Drosophila melanogaster

In many insects, females exhibit behavioral changes after mating. This plasticity can be mediated by interactions between male-derived seminal fluid proteins (SFPs) and the female nervous system. The Drosophila melanogaster seminal fluid protein Sex Peptide (SP) causes mated females to sleep less during the day and consume more food than unmated females, among other behavioral changes. Although the SP-sensing neural circuits that convey information to the females brain are known, the downstream neurons that affect post-mating behaviors remain unknown. P2 neurons in the flys central brain are good candidates for regulating post-mating changes in sleep and food consumption, as they express feeding- and sleep-responsive neuropeptide F (NPF), directly innervate the flys sleep center (the dorsal fan-shaped body, dFB), and are responsible for social-isolation-induced changes in sleep and food consumption. Using the GAL4/UAS system, we activated or silenced P2 neurons in mated and unmated females. We measured sleep duration using Drosophila Activity Monitors (DAM) and food consumption using Capillary Feeder (CAFE) and blue-dye assays. We found that P2-neurons are not responsible for post-mating changes in sleep and food consumption: mated females slept less during the day and ate more compared to unmated females irrespective of P2 neuron perturbation. Together, these results indicate that P2 neurons are unlikely to be primary downstream neurons through which male-transferred SP regulates post-mating sleep and food consumption. Future studies could determine whether P2 neurons regulate other post-mating behaviors or modulate sleep and feeding behaviors in a context-dependent manner.

genetics↗

bioRxiv2023

The Drosophila melanogaster Y-linked gene, WDY, is required for sperm to swim in the female reproductive tract.

Unique patterns of inheritance and selection on Y chromosomes lead to the evolution of specialized gene functions. Yet characterizing the function of genes on Y chromosomes is notoriously difficult. We report CRISPR mutants in Drosophila of the Y-linked gene, WDY, which is required for male fertility. WDY mutants produce mature sperm with beating tails that can be transferred to females but fail to enter the female sperm storage organs. We demonstrate that the sperm tails of WDY mutants beat approximately half as fast as wild-type sperms and that the mutant sperm do not propel themselves within the male ejaculatory duct or female reproductive tract (RT). These specific motility defects likely cause the sperm storage defect and sterility of the mutants. Regional and genotype-dependent differences in sperm motility suggest that sperm tail beating and propulsion do not always correlate. Furthermore, we find significant differences in the hydrophobicity of key residues of a putative calcium-binding domain between orthologs of WDY that are Y-linked and those that are autosomal. Given that WDY appears to be evolving under positive selection, our results suggest that WDYs functional evolution coincides with its transition from autosomal to Y-linked in Drosophila melanogaster and its most closely related species. Finally, we show that mutants for another Y-linked gene, PRY, also show a sperm storage defect that may explain their subfertility. In contrast to WDY, PRY mutants do swim in the female RT, suggesting they are defective in yet another mode of motility, navigation, or a necessary interaction with the female RT. Overall, we provide direct evidence for the long-held presumption that protein-coding genes on the Drosophila Y regulate sperm motility.

genetics↗

bioRxiv2020

CRISPR Mutants of Three Y Chromosome Genes Suggest Gradual Evolution of Fertility Functions in Drosophila melanogaster

Gene-poor, repeat-rich regions of the genome are poorly understood and have been understudied due to technical challenges and the misconception that they are degenerating "junk". Yet multiple lines of evidence indicate these regions may be an important source of variation that could drive adaptation and species divergence, particularly through regulation of fertility. The [~]40 Mb Y chromosome of Drosophila melanogaster contains only 16 known protein-coding genes and is highly repetitive and entirely heterochromatic. Most of the genes originated from duplication of autosomal genes and have reduced nonsynonymous substitution rates, suggesting functional constraint. We devised a genetic strategy for recovering and retaining stocks with sterile Y-linked mutations and combined it with CRISPR to create mutants with deletions that disrupt three Y-linked genes. Two genes, PRY and FDY, had no previously identified functions. We found that PRY mutant males are sub-fertile, but FDY mutant males had no detectable fertility defects. FDY, the newest known gene on the Y chromosome, may have fertility effects that are conditional or too subtle to detect. The third gene, CCY, had been predicted but never formally shown to be required for male fertility. CRISPR-targeting and RNAi of CCY caused male sterility. Surprisingly, however, our CCY mutants were sterile even in the presence of an extra wild-type Y chromosome, suggesting that perturbation of the Y chromosome can lead to dominant sterility. Our approach provides an important step toward understanding the complex functions of the Y chromosome and parsing which functions are accomplished by genes versus repeat elements.

genetics↗