About

Rupinder Kaur is an Assistant Research Professor at the Department of Entomology at Penn State University. Her research focuses on insect science, an interdisciplinary life science that aims to improve human health, quality of life, and the sustainability of food and ecosystems. As part of the department's community of faculty, staff, and students, she contributes to research efforts that support these goals.

Research topics

• Biology
• Genetics
• Evolutionary biology
• Ecology
• Cell biology

Selected publications

• Cytoplasmic incompatibility factor proteins from <i>Wolbachia</i> prophage are costly to sperm development in <i>Drosophila melanogaster</i>

  Proceedings of the Royal Society B Biological Sciences · 2025-02-01 · 1 citations

  articleOpen access1st authorCorresponding

  The symbiosis between arthropods and Wolbachia bacteria is globally widespread, largely due to selfish-drive systems that favour the fitness of symbiont-transmitting females. The most common drive, cytoplasmic incompatibility (CI), is central to arboviral control efforts. In Drosophila melanogaster carrying w Mel Wolbachia deployed in mosquito control, two prophage genes in Wolbachia, cifA and cifB , cause CI that results in a paternal-effect lethality of embryos in crosses between Wolbachia -bearing males and aposymbiotic females. While the CI mechanism by which Cif proteins alter sperm development has recently been elucidated in D. melanogaster and Aedes aegypti mosquitoes, the Cifs’ extended impact on male reproductive fitness such as sperm morphology and quantity remains unclear. Here, using cytochemical, microscopic and transgenic assays in D. melanogaster, we demonstrate that both CifA and CifB cause a significant portion of defects in elongating spermatids, culminating in malformed mature sperm nuclei. Males expressing Cifs have reduced spermatid bundles and sperm counts, and transgenic expression of Cifs can occasionally result in no mature sperm formation. We reflect on Cifs’ varied functional impacts on the Host Modification model of CI as well as host evolution, behaviour and vector control strategies.

  PublisherDOI

• Evolutionary Diversification and Functions of the Candidate Male Killing Gene <i>wmk</i>

  Genome Biology and Evolution · 2025-09-19 · 2 citations

  articleOpen access

  Symbiont-mediated male killing (MK) is a mechanism that selectively eliminates male offspring, often by disrupting sex-specific developmental processes. In Drosophila melanogaster, the WO-mediated killing gene wmk from Wolbachia prophage WO transgenically reproduces the MK phenotype, yet how the gene evolves and functions across diverse Wolbachia has not been systematically investigated. We analyzed 32 Wolbachia genomes available in the NCBI database to study wmk homologs across different arthropod hosts, reproductive parasitism functions, and Wolbachia supergroups. First, we report at least five distinct wmk phylogenetic clusters (Types I to V), often organized in multigenic dyads or triads. Second, among MK Wolbachia, there is a significantly higher number of wmk genes and diversity in Lepidoptera strains than in Drosophila strains, which exclusively harbor wmk Types I and III. Third, there are three patterns of wmk sequence and genomic organizational changes in Drosophila MK strains that associate with different evolutionary trajectories underpinning the MK phenotype. Fourth, single and combinatory transgenic expression of Types I and III in D. melanogaster uncovers male-biased lethality associated with Type I; however, dual expression of the Types together elicits a major reduction in offspring number. Fifth, wmk genes have low expression level across D. melanogaster developmental stages relative to the cifA and cifB genes, which could explain why cytoplasmic incompatibility is expressed in this system. These findings establish a complex and phylogenetically informed genetic basis of wmk-induced lethality, highlighting the role of gene copy number and expression, wmk Types, and host background in shaping the phenotype.

  PublisherDOI

• Histone acetylation modulation by a small molecule inhibitor recapitulates symbiont-induced cytoplasmic incompatibility

  Cell Reports · 2025-10-01 · 2 citations

  articleOpen access1st authorCorresponding

  Symbiotic relationships between arthropod hosts and microorganisms have garnered global attention for their influence on host ecology, evolution, and vector control. A major gap in the field is to mechanistically define and reconstitute symbiotic traits in the absence of microbes. Here, we address this omission by identifying an evolutionarily conserved host mechanism that recapitulates Wolbachia-induced cytoplasmic incompatibility (CI)-a paternal-effect embryonic lethality trait. We first show that Wolbachia alter histone acetylation during sperm development in Drosophila melanogaster. By chemically inhibiting histone acetyltransferase (HAT) activity in aposymbiotic males, we reprogram the chromatin landscape of developing sperm to induce a rescuable CI phenotype. This phenotype is further modulated through transgenic knockdown of HAT and histone deacetylase enzymes, providing tunable control over natural CI intensity. Our findings uncover histone acetylation as a key host-intrinsic pathway, capable of inducing symbiont-independent CI for new avenues of basic and applied studies.

  PublisherDOI

• The mechanism of cytoplasmic incompatibility is conserved in Wolbachia-infected Aedes aegypti mosquitoes deployed for arbovirus control

  PLoS Biology · 2024-03-28 · 15 citations

  articleOpen access1st authorCorresponding

  The rising interest and success in deploying inherited microorganisms and cytoplasmic incompatibility (CI) for vector control strategies necessitate an explanation of the CI mechanism. Wolbachia-induced CI manifests in the form of embryonic lethality when sperm from Wolbachia-bearing testes fertilize eggs from uninfected females. Embryos from infected females however survive to sustain the maternally inherited symbiont. Previously in Drosophila melanogaster flies, we demonstrated that CI modifies chromatin integrity in developing sperm to bestow the embryonic lethality. Here, we validate these findings using wMel-transinfected Aedes aegypti mosquitoes released to control vector-borne diseases. Once again, the prophage WO CI proteins, CifA and CifB, target male gametic nuclei to modify chromatin integrity via an aberrant histone-to-protamine transition. Cifs are not detected in the embryo, and thus elicit CI via the nucleoprotein modifications established pre-fertilization. The rescue protein CifA in oogenesis localizes to stem cell, nurse cell, and oocyte nuclei, as well as embryonic DNA during embryogenesis. Discovery of the nuclear targeting Cifs and altered histone-to-protamine transition in both Aedes aegypti mosquitoes and D. melanogaster flies affirm the Host Modification Model of CI is conserved across these host species. The study also newly uncovers the cell biology of Cif proteins in the ovaries, CifA localization in the embryos, and an impaired histone-to-protamine transition during spermiogenesis of any mosquito species. Overall, these sperm modification findings may enable future optimization of CI efficacy in vectors or pests that are refractory to Wolbachia transinfections.

  PublisherOA PDFDOI

• Gut-Germline Axis: A Reproductive Endosymbiont's Adaptation is Modulated by the Gut Microbiome

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-09-10 · 4 citations

  preprintOpen access

  Holobionts contain extra- and intracellular microbes that are typically studied in symbiotic and anatomical siloes. Here we demonstrate a previously unknown impact of the extracellular gut microbiome on the adaptation of a reproductive endosymbiont. Specifically, a paternal-effect embryonic lethality caused by Wolbachia-induced cytoplasmic incompatibility (CI) is attenuated by the gut microbiome. Gut microbiome-mediated variation in the CI phenotype causes key gene expression changes in the symbiosis and defining cell biological defects in the evolutionary conserved histone-to-protamine transition that drives CI. Reintroducing the gut microbiome into germ-free flies recapitulates the CI attenuation. Notably, the integrated holobiont exhibits significantly elevated gut microbiome and endosymbiont densities relative to isolated constituent rearing, highlighting a synergistic relationship. Finally, impacts of the symbionts on survival are independent and inversely related throughout development, and fitness changes are recapitulated when the gut microbiome is restored. Altogether, this study uncovers a gut-germline axis in which bacteria shape an entangled network of symbiotic functions within a holobiont. Interorgan, symbiotic relationships have far-reaching implications for the study of trait variation.

  PublisherDOI

• Prophage proteins alter long noncoding RNA and DNA of developing sperm to induce a paternal-effect lethality

  Science · 2024-03-07 · 26 citations

  articleOpen access1st authorCorresponding

  The extent to which prophage proteins interact with eukaryotic macromolecules is largely unknown. In this work, we show that cytoplasmic incompatibility factor A (CifA) and B (CifB) proteins, encoded by prophage WO of the endosymbiont Wolbachia, alter long noncoding RNA (lncRNA) and DNA during Drosophila sperm development to establish a paternal-effect embryonic lethality known as cytoplasmic incompatibility (CI). CifA is a ribonuclease (RNase) that depletes a spermatocyte lncRNA important for the histone-to-protamine transition of spermiogenesis. Both CifA and CifB are deoxyribonucleases (DNases) that elevate DNA damage in late spermiogenesis. lncRNA knockdown enhances CI, and mutagenesis links lncRNA depletion and subsequent sperm chromatin integrity changes to embryonic DNA damage and CI. Hence, prophage proteins interact with eukaryotic macromolecules during gametogenesis to create a symbiosis that is fundamental to insect evolution and vector control.

  PublisherOA PDFDOI

• Transgenic cytoplasmic incompatibility persists across age and temperature variation in Drosophila melanogaster

  iScience · 2022-10-10 · 3 citations

  articleOpen access

  transgenes.

  PublisherOA PDFDOI

• The Cif proteins from Wolbachia prophage WO modify sperm genome integrity to establish cytoplasmic incompatibility

  PLoS Biology · 2022 · 53 citations

  1st authorCorresponding
  • Biology
  • Genetics
  • Cell biology

  Inherited microorganisms can selfishly manipulate host reproduction to drive through populations. In Drosophila melanogaster, germline expression of the native Wolbachia prophage WO proteins CifA and CifB cause cytoplasmic incompatibility (CI) in which embryos from infected males and uninfected females suffer catastrophic mitotic defects and lethality; however, in infected females, CifA expression rescues the embryonic lethality and thus imparts a fitness advantage to the maternally transmitted Wolbachia. Despite widespread relevance to sex determination, evolution, and vector control, the mechanisms underlying when and how CI impairs male reproduction remain unknown and a topic of debate. Here, we use cytochemical, microscopic, and transgenic assays in D. melanogaster to demonstrate that CifA and CifB proteins of wMel localize to nuclear DNA throughout the process of spermatogenesis. Cif proteins cause abnormal histone retention in elongating spermatids and protamine deficiency in mature sperms that travel to the female reproductive tract with Cif proteins. Notably, protamine gene knockouts enhance wild-type CI. In ovaries, CifA localizes to germ cell nuclei and cytoplasm of early-stage egg chambers; however, Cifs are absent in late-stage oocytes and subsequently in fertilized embryos. Finally, CI and rescue are contingent upon a newly annotated CifA bipartite nuclear localization sequence. Together, our results strongly support the Host modification model of CI in which Cifs initially modify the paternal and maternal gametes to bestow CI-defining embryonic lethality and rescue.

  PublisherOA PDFDOI

• Nuclease proteins CifA and CifB promote spermatid DNA damage associated with symbiont-induced cytoplasmic incompatibility

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-04-04 · 8 citations

  preprintOpen access1st authorCorresponding

  Summary The worldwide endosymbiosis between arthropods and Wolbachia bacteria is an archetype for reproductive parasitism. This parasitic strategy rapidly increases the proportion of symbiont-transmitting mothers, and the most common form, cytoplasmic incompatibility (CI), impacts insect evolution and arboviral control strategies. During CI, sperms from symbiotic males kill embryos of aposymbiotic females via two nuclear-targeting proteins, CifA and CifB, that alter sperm chromatin organization in Drosophila melanogaster . Here we hypothesize that Cif proteins metabolize nucleic acids of developing sperm to initiate genome integrity changes. Using in vitro and in situ transgenic, mutant, enzymatic, and cytochemical assays, we show that CifA is a previously-unrecognized DNase and RNase, and CifB is a DNase. Notably, in vitro nuclease activity translates to in situ spermatid DNA damage at the canoe stage of spermiogenesis. Evolution-guided mutations ablate Cif enzymatic activity. Nucleic acid metabolism by Cif enzymes expands a fundamental understanding of the mechanism of symbiont-mediated reproductive parasitism.

  PublisherOA PDFDOI

• The Cif proteins from <i>Wolbachia</i> prophage WO modify sperm genome integrity to establish cytoplasmic incompatibility

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-01-16 · 3 citations

  preprintOpen access1st author

  Abstract Inherited microorganisms can selfishly manipulate host reproduction to drive through populations. In Drosophila melanogaster , germline expression of the native Wolbachia prophage WO proteins CifA and CifB cause cytoplasmic incompatibility (CI) in which embryos from infected males and uninfected females suffer catastrophic mitotic defects and lethality; however, in infected females, CifA expression rescues the embryonic lethality and thus imparts a fitness advantage to the maternally-transmitted Wolbachia . Despite widespread relevance to sex determination, evolution, and vector control, the mechanisms underlying when and how CI impairs male reproduction remain unknown and a topic of debate. Here we use cytochemical, microscopic, and transgenic assays in D. melanogaster to demonstrate that CifA and CifB proteins of w Mel localize to nuclear DNA throughout the process of spermatogenesis. Cif proteins cause abnormal histone retention in elongating spermatids and protamine deficiency in mature sperms that travel to the female reproductive tract with Cif proteins. Notably, protamine gene knockouts enhance wild type CI. In ovaries, CifA localizes to germ cell nuclei and cytoplasm of early-stage egg chambers, however Cifs are absent in late-stage oocytes and subsequently in fertilized embryos. Finally, CI and rescue are contingent upon a newly annotated CifA bipartite nuclear localization sequence. Together, our results strongly support the Host Modification model of CI in which Cifs initially modify the paternal and maternal gametes to bestow CI-defining embryonic lethality and rescue.

  PublisherOA PDFDOI

Frequent coauthors

• Seth R. Bordenstein

  Pennsylvania State University

  27 shared

• Brittany A. Leigh

  Vanderbilt University

  12 shared

• Omar Rota‐Stabelli

  University of Trento

  11 shared

• Wolfgang J. Miller

  Medical University of Vienna

  9 shared

• J. Dylan Shropshire

  Vanderbilt University

  8 shared

• Mitali Mukerji

  Indian Institute of Integrative Medicine

  7 shared

• Manickam Chidambaram

  7 shared

• Isabella T. Ritchie

  University of South Florida St. Petersburg

  7 shared

Labs

• Christina Grozinger LabPI

Education

• Ph.D.

  University of Vienna, Austria