Biology subjects

Phadnis, N.

Publications and source records attributed to Phadnis, N..

4 recordsLinked to original sources

bioRxiv2018

Altered chromatin localization of hybrid lethality proteins in Drosophila

Understanding hybrid incompatibilities is a fundamental pursuit in evolutionary genetics. In crosses between Drosophila melanogaster females and Drosophila simulans males, the interaction of at least three genes is necessary for hybrid male lethality: Hmr mel, Lhr sim, and gfzf sim. All three hybrid incompatibility genes are chromatin associated factors. While HMR and LHR physically bind each other and function together in a single complex, the connection between either of these proteins and gfzf remains mysterious. Here, we investigate the allele specific chromatin binding patterns of gfzf. First, our cytological analyses show that there is little difference in protein localization of GFZF between the two species except at telomeric sequences. In particular, GFZF binds the telomeric retrotransposon repeat arrays, and the differential binding of GFZF at telomeres reflects the rapid changes in sequence composition at telomeres between D. melanogaster and D. simulans. Second, we investigate the patterns of GFZF and HMR co-localization and find that the two proteins do not normally co-localize in D. melanogaster. However, in inter-species hybrids, HMR shows extensive mis-localization to GFZF sites, and this altered localization requires the presence of gfzf sim. Third, we find by ChIP-Seq that over-expression of HMR and LHR within species is sufficient to cause HMR to mis-localize to GFZF binding sites, indicating that HMR has a natural low affinity for GFZF sites. Together, these studies provide the first insights into the different properties of gfzf between D. melanogaster and D. simulans as well as a molecular interaction between gfzf and Hmr in the form of altered protein localization.

molecular biology↗

bioRxiv2018

Rampant cryptic sex chromosome drive in Drosophila

Theory predicts that selfish genetic elements that increase their transmission are prone to originate on sex chromosomes but create strong selective pressure to evolve suppressors due to reduced fertility and distorted population sex ratios. Here we show that recurrent genetic conflict over sex chromosome transmission appears to be an important evolutionary force that has shaped gene content evolution of sex chromosomes in Drosophila. We demonstrate that convergent acquisition and amplification of spermatid expressed gene families are common on Drosophila sex chromosomes, and especially on recently formed ones, and harbor characteristics typical of meiotic drivers. We carefully characterize one putative novel cryptic sex chromosome distortion system that arose independently several times in members of the Drosophila obscura group. Co-amplification of the S-Lap1/GAPsec gene pair on both the X and the Y chromosome occurred independently several times in members of the D. obscura group, where this normally autosomal gene pair is sex-linked due to a sex chromosome - autosome fusion. Investigation of gene expression and short RNA profiles at the S-Lap1/GAPsec system suggest that meiotic drive and suppression likely involves RNAi mechanisms. Our finding suggests that recurrent conflict over sex chromosome transmission has shaped widespread genomic and evolutionary patterns, including the epigenetic regulation of sex chromosomes, the distribution of sex-biased genes, and the evolution of hybrid sterility.

genomics↗

bioRxiv2017

The role of chromosomal inversions in speciation

The chromosomal inversions of D. persimilis and D. pseudoobscura have deeply influenced our understanding of the evolutionary forces that shape natural variation, speciation, and selfish chromosome dynamics. Here, we perform a comprehensive reconstruction of the evolutionary histories of the chromosomal inversions in these species. We provide a solution to the puzzling origins of the selfish Sex-Ratio chromosome in D. persimilis and show that this Sex-Ratio chromosome directly descends from an ancestrally-arranged chromosome. Our results further show that all fixed inversions between D. persimilis and D. pseudoobscura were segregating in the ancestral population long before speciation, and that the genes contributing to reproductive barriers between these species must have evolved within them afterwards. We propose a new model for the role of chromosomal inversions in speciation and suggest that higher levels of divergence and an association with hybrid incompatibilities are emergent properties of ancestrally segregating inversions. These findings force a reconsideration of the role of chromosomal inversions in speciation, not as protectors of existing hybrid incompatibility alleles, but as fertile grounds for their formation.

evolutionary biology↗

bioRxiv2017

Parallel evolution of sperm hyper-activation Ca2+ channels

Sperm hyper-activation is a dramatic change in sperm behavior where mature sperm burst into a final sprint in the race to the egg. The mechanism of sperm hyper-activation in many metazoans, including humans, consists of a jolt of Ca2+ into the sperm flagellum via CatSper ion channels. Surprisingly, CatSper genes have been independently lost in several animal lineages. In Drosophila, sperm hyper-activation is performed through the co-option of the polycystic kidney disease 2 (Dpkd2) Ca2+ channel. The parallels between CatSpers in primates and Dpkd2 in Drosophila provide a unique opportunity to examine the molecular evolution of the sperm hyper-activation machinery in two independent, nonhomologous calcium channels separated by more than 500 million years of divergence. Here, we use a comprehensive phylogenomic approach to investigate the selective pressures on these sperm hyper-activation channels. First, we find that the entire CatSper complex evolves rapidly under recurrent positive selection in primates. Second, we find that pkd2 has parallel patterns of adaptive evolution in Drosophila. Third, we show that this adaptive evolution of pkd2 is driven by its role in sperm hyper-activation. These patterns of selection suggest that the evolution of the sperm hyper-activation machinery is driven by sexual conflict with antagonistic ligands that modulate channel activity. Together, our results add sperm hyper-activation channels to the class of fast evolving reproductive proteins and provide insights into the mechanisms used by the sexes to manipulate sperm behavior.

evolutionary biology↗