Piyali Mukherjee

Assistant Professor and Coordinator, Institute of Health Sciences

One of the major questions that have driven my research interest throughout my scientific career is to understand the triggers of cell death and survival. To pursue some of the intriguing questions in biology our laboratory at the Institute of Health Sciences are currently working on the following projects:

Role of  the PARP1/Sirtuin/Sarm1 axis in the regulation of mitochondrial homeostasis in aging and  neurodegeneration

Mitochondria which are determinants of both ‘cell survival’ through the synthesis of ATP as well as ‘cell death’ by mediating apoptosis is the central theme to our ongoing projects. We are currently trying to understand the balance between cell death and survival mechanisms in the context of cellular metabolism with particular emphasis on the NAD+ pathway. The molecule of interest is Sarm1 (sterile alpha and TIR containing protein 1) which is a central regulator of programmed axonal degeneration. We have recently shown that early loss of NAD+ via PARP1 hyperactivation following mitochondrial complex I inhibition leads to defective mitophagy and Sarm1 induction. We are trying to connect  how the NAD+ consuming enzymes like PARP1, Sirtuins as well as the pro-neurodegenerative molecule Sarm1 plays a role in neuronal cell death under mitochondrial complex I inhibition or in aging using both neuronal cell lines as well the model organism Drosophila melanogaster.

Host-Pathogen interaction

We are currently pursuing two questions to understand how the host innate immune response plays a determining role in the disease outcome:

i. Understanding the role of mitochondrial innate immune regulation during neurotropic virus infection

The first line of defense against a viral infection is to mount a productive Type-I interferon response that limits viral replication within host cells. Innate immune recognition of RNA viruses involves interactions at the mitochondria resulting in tradeoffs between efficiency vs fidelity of responses. While signaling via the MAVS signalosome is essential to limit viral replication it must also be stringently controlled to prevent hyperstimulation of immune responses. How this can be achieved? One negative regulator of MAVS is the pro-neurodegenerative molecule Sarm1, a member of the TLR adaptor family of proteins. Whether this is a strategy of the host to prevent axonal spread of viruses within the CNS or a subversion strategy adopted by the viruses to dampen MAVS-mediated interferon responses is an intriguing question that is the focus of our research using the neurotropic Chandipura virus (CHPV) as the model system.

ii. Role of the cGAS-STING pathway in cervical cancer

Cervical cancer which is the 4th most common cancer of women worldwide is caused by the persistence of high-risk HPV16 (~50%) or HPV18 (~15%) infection and HPV DNA is detectable in 90% of affected tissue. In recent years a host innate defense mechanism against invading DNA viruses have emerged that involve recognition of the cytosolic DNA by the receptor cGAS resulting in the production of the second messenger cGAMP which stimulates the receptor STING for the production of Type I interferons. Many viruses have evolved strategies of immune evasion by the cGas- STING pathways either via the masking of DNA ligands, post translational modification of STING or degradation of cGAMP. We are trying to elucidate the regulation of the cGAS-STING pathway in HPV-induced cervical cancer and gain a preliminary insight into the STING variants in Indian cervical cancer patients.


Presidency University,
86/1 College Street, Kolkata - 700073,
West Bengal, India

CV Not Available
Email: piyali.biochem at presiuniv.ac.in
alternate E-mail: piyali.dbs at presiuniv.ac.in

How to Find Us

Presidency University
(Main Campus)

86/1 College Street
Kolkata 700073

Presidency University
(2nd Campus)

Plot No. DG/02/02,
Premises No. 14-0358, Action Area-ID
New Town
(Near Biswa Bangla Convention Centre)
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