PhD in Yeast Molecular Genetics (1996-2001): School of Life Sciences, Jawaharlal Nehru University, New Delhi.
Bsc Biochemistry (Hons.) (1989-1992): Sri Venkateswara College, University of Delhi
Msc Biochemistry (1992-1994): University of Delhi South Campus
Areas of Interest/Specialization
Candida albicans is a natural component of the human flora that can cause life-threatening infections in immunosuppressed patients. Treatment of fungal infections is a challenge due to the limited repertoire of available antifungals. Additionally, both the planktonic as well as biofilm modes of growth of C. albicans develop resistance to existing azole antifungals due to the upregulation of drug efflux pumps, posing a challenge in treating Candida infections. This necessitates the need to identify additional cellular targets for antifungal therapy. In this context, our lab focuses on dissecting various cellular processes that are regulated by the mitochondria and the seven-transmembrane receptor family of proteins (Rta2, Rta3 and Rta4), in an attempt to identify features that are unique to C. albicans. We propose that targeting the mitochondria and the Rta family of proteins will increase the antifungal target space and will provide powerful strategy to treat fungal infections. We have shown that mitochondria are required for modulating drug resistance, lipid homeostasis, Hog1-mediated oxidative stress pathway, iron homeostasis and ergosterol levels in C. albicans.
The Rta1-like family in S. cerevisiae was initially named LTE, for lipid-translocating exporter, based on the finding that Rsb1 is involved in the release of sphingoid bases. In C. albicans Rta1 family of proteins are unique to fungal kingdom and can be considered as potential therapeutic targets. Functional analysis of the Rta1 family of proteins has revealed their importance in regulating a plethora of functions such as modulating ER stress response and asymmetric distribution of phosphatidylcholine across the plasma membrane. Additionally we show that all these proteins are involved in regulating biofilm formation in C. albicans. Considering that biofilm-specific drugs do not exist in C. albicans, targeting these genes may have therapeutic implications that may contribute to the development of biofilm-specific antifungals.