Our research broadly explores the mechanistic basis of the diverse strategies microbes use to shape host biology, reproduction, behavior, and disease outcomes. Our model is the symbiotic bacterium Wolbachia, which is unculturable, and therefore, we study its biology through the lens of its insect hosts. By dissecting the molecular and epigenetic mechanisms through which Wolbachia reprograms host physiology, we aim to understand how these interactions can be harnessed for translational applications in public health and biotechnology.

Wolbachia — the maternally transmitted, obligately intracellular bacteria present in ~50% of arthropod species — primarily reside in reproductive tissues and manipulate host reproduction to favor its own transmission via infected females. The most common manipulation known as cytoplasmic incompatibility (CI) causes embryonic lethality when sperm from infected males fertilize uninfected eggs, while infected females rescue this lethality and pass the bacteria to offspring. Coupled with Wolbachia’s ability to block RNA viruses such as dengue, Zika, West Nile and Chikungunya, CI has become a cornerstone of vector control strategies as it favours the spreading of Wolbachia in vector populations through the elimination of uninfected eggs and renders them refractory to virus replication and transmission. The World Health Organization has recognized and endorsed the public health value of future Wolbachia research to curb dengue, for example.

Since Wolbachia’s success in vector control programs heavily relies on CI, Dr. Kaur pioneered in investigating how Wolbachia proteins interact with host reproductive and developmental pathways to control sperm development, fertilization outcome, and offspring viability. Her work has shown that CI-inducing factors (CifA and CifB) invade developing sperm nuclei, deplete long non-coding RNAs, promote DNA damage, and disrupt the histone-to-protamine transition — an epigenetically regulated process critical for male fertility. With these modifications, the altered sperm causes embryonic death by likely accumulating fatal DNA replication errors during mitotic divisions. Building on this knowledge and harnessing the power of synthetic/chemical biology, she has led efforts to engineer Wolbachia-modulated epigenetic pathway in an uninfected host to recapitulate reproductive symbiotic phenotype.

While the mechanistic understanding of CI is now well understood and continues to be developing across systems, the mechanism of rescue that enables Wolbachia spread in host population remains unknown, limiting our ability to optimize, control, or extend this strategy. Dr. Kaur's previous findings show that infected females carrying CifA can rescue embryonic lethality by interacting with maternal chromatin during oogenesis as well as embryogenesis, however, CifA-mediated maternal chromatin alterations remain unexplored. The lab will continue pulling at this thread to further investigate:

Another arm of our lab's research will aim to investigate how Wolbachia block viral pathogens in mosquitoes, a transformative avenue for disease control. While multiple host and bacterial factors contribute to antiviral resistance, the role of prophage-encoded factors — often termed the “Warhead of Wolbachia” — remains largely unexplored. It is also unclear why some Wolbachia strains confer resistance to certain viruses while others do not, or why some viruses are suppressed and others are enhanced in the presence of Wolbachia, and how these different Wolbachia-virus combinations interact within the host cellular environment to shape these outcomes. Using transgenics, synthetic biology, high-throughput sequencing, and functional assays, the lab aims to decode the mechanisms by which Wolbachia suppress viruses and design customizable biocontrol tools that strengthen virus-blocking capabilities.