Amruta Bhate

Biochemistry Graduate Student

School of Molecular Cell Biology

B.S. Biochemistry - University of Mumbai

Worked in the Lab: December 2012 - July 2017

Current Position: Post-doc Fellow at UCSF


Funding: Herbert L. Carter fellowship in Biochemistry


Bhate A*, Parker DJ*, Bebee TW, Ahn J, Arif W, Rashan EH, Chorghade S, Chau A, Lee JH, Anakk S, Carstens RP, Xiao X and Kalsotra A (2015) ESRP2 controls an adult splicing program in hepatocytes to support postnatal liver maturation. Nat. Commun. 6:8768 | DOI: 10.1038/ncomms9768 | * denotes equal authors

Alam H., Bhate A., Gangadaran P., Sawant S., Sehgal L., Salot S., Dange P., Chaukar D., D’cruz A., Kannan S., Gude R., Dalal S. And Vaidya M. ‘Fascin overexpression promotes neoplastic progression in OSCC.’ BMC Cancer 12:32. doi: 10.1186/1471-2407-12-32.

Alam H., Gangadaran P, Bhate A, Chaukar DA, Sawant SS, Tiwari R, Bobade J, Kannan S, D’cruz AK, Kane S And Vaidya MM. ‘Loss of Kertain 8 phosphorylation leads to increased tumour progression and correlates with clinicopathological parameters of OSCC patients.’ PLoS One 6(11):e27767. doi: 10.1371.


(Click images to enlarge)

I am a Ph.D student in the Biochemistry Department. I hail from Mumbai, India. I have an undergrad degree in Biochemistry from the University of Mumbai. I love reading, it is hard for me to put down a book (a good one or otherwise) once I start reading! I love travelling, and my dream is to backpack across Europe! I also like learning new languages.

During my undergrad, I had the opportunity to work in an oral cancer lab at ACTREC, Navi Mumbai where I had a chance to study closely how malfunction of cellular mechanisms can lead to malignancies. This further deepened my interest in studying the mechanisms/regulatory networks which control gene expression and determine cell and tissue function.

Alternative splicing (AS) is the most prominent mechanism to generate mRNA complexity which in turn results in increased proteome diversity. Liver is the major metabolic organ of the body which undergoes massive developmental transitions with regards to function and structure. Thus, I want to study the role of alternative pre-mRNA splicing in liver development. My long term goal is to identify the determinants of AS which drive developmental transitions in liver and characterize the functional role of certain RNA binding proteins like MBNL1, CELF1 in liver development.

Currently I am performing a genome-wide analysis of AS events during mammalian liver development to identify conserved and co-ordinately regulated events. During my preliminary analysis, I have screened ~150 events, based on the RNA-Seq experiment performed in the lab to check for the same (Fig.1 F,G), at two developmental timepoints; E18 and PN28 in mice and found that almost 80% of these events show a significant change in splicing pattern. This screening will eventually help us determine the gene pathways that undergo splicing during liver development. Using the Cre-lox Tissue specific/conditional knock-out mouse models for certain RNA Binding Proteins, which are being developed in the lab, we would be able to identify the splicing regulators which might be associated in the regulation of the splicing program during liver development.