Ph.D, MSc, BSc

Dr. Priyanka Somanath serves as Assistant Professor in the School of Biotechnology. Dr. Priyanka Somanath obtained her Ph.D. from the University of California, Davis, USA, where she worked on elucidating the molecular functions of pluripotency-specific proteins in embryonic stem cells and their relationship to cancer. Additionally, she utilized the genome editing strategy, CRISPR-Cas9, to determine the unique functions of core epigenetic proteins in gene regulation of human cells. She also served as lead Teaching Assistant in multiple undergraduate courses at UC Davis.

Dr. Somanath has research experience from several international universities including the University of California, Berkeley and The Hong Kong University of Science and Technology, where she worked on three-dimensional cell culture systems and cell cycle control in human cancer cells. She also has past research experience working in the biotechnology industry at Genentech, Inc., USA.

2017 Ph.D. Biochemistry, Molecular, Cell and Developmental Biology University of California, Davis, USA
2008 M.Sc. Biotechnology Amrita School of Biotechnology
2006 B.Sc. Microbiology/Chemistry University of Mysore

Selected Presentations

  • Poster presentation titled “A DPPA4-interacting protein network in pluripotent and cancer cells” at the International Society for Stem Cell Research (ISSCR) Annual Meeting 2016 – San Francisco, CA, USA.


  • Silver Medal- M.Sc., Amrita Vishwa Vidyapeetham.
  • Alamelammal H Ramanujan Iyengar Gold Medal- B.Sc., University of Mysore.


Publication Type: Journal Article

Year of Publication Publication Type Title


Journal Article

Priyanka Somanath, Bush, K. M., and Knoepfler, P. S., “ERBB3-Binding Protein 1 (EBP1) Is a Novel Developmental Pluripotency-Associated-4 (DPPA4) Cofactor in Human Pluripotent Cells”, STEM CELLS, p. n/a–n/a, 2018.[Abstract]

Developmental Pluripotency-Associated-4 (DPPA4) is one of the few core pluripotency genes lacking clearly defined molecular and cellular functions. Here, we used a proteomics screening approach of human embryonic stem cell (hESC) nuclear extract to determine DPPA4 molecular functions through identification of novel cofactors. Unexpectedly, the signaling molecule ERBB3-binding protein 1 (EBP1) was the strongest candidate binding partner for DPPA4 in hESC. EBP1 is a growth factor signaling mediator present in two isoforms, p48 and p42. The two isoforms generally have opposing functions, however their roles in pluripotent cells have not been established. We found that DPPA4 preferentially binds p48 in pluripotent and NTERA-2 cells, but this interaction is largely absent in non-pluripotent cells and is reduced with differentiation. The DPPA4–EBP1 interaction is mediated at least in part in DPPA4 by the highly conserved SAF-A/B, Acinus and PIAS (SAP) domain. Functionally, we found that DPPA4 transcriptional repressive function in reporter assays is significantly increased by specific p48 knockdown, an effect that was abolished with an interaction-deficient DPPA4 ΔSAP mutant. Thus, DPPA4 and EBP1 may cooperate in transcriptional functions through their physical association in a pluripotent cell specific context. Our study identifies EBP1 as a novel pluripotency cofactor and provides insight into potential mechanisms used by DPPA4 in regulating pluripotency through its association with EBP1. Stem Cells 2018

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Journal Article

Priyanka Somanath, Klein, R. Herndon, and Knoepfler, P. S., “CRISPR-mediated HDAC2 disruption identifies two distinct classes of target genes in human cells”, PLOS ONE, vol. 12, pp. 1-21, 2017.[Abstract]

The transcriptional functions of the class I histone deacetylases (HDACs) HDAC1 and HDAC2 are mainly viewed as both repressive and redundant based on murine knockout studies, but they may have additional independent roles and their physiological functions in human cells are not as clearly defined. To address the individual epigenomic functions of HDAC2, here we utilized CRISPR-Cas9 to disrupt HDAC2 in human cells. We find that while HDAC2 null cells exhibited signs of cross-regulation between HDAC1 and HDAC2, specific epigenomic phenotypes were still apparent using RNA-seq and ChIP assays. We identified specific targets of HDAC2 repression, and defined a novel class of genes that are actively expressed in a partially HDAC2-dependent manner. While HDAC2 was required for the recruitment of HDAC1 to repressed HDAC2-gene targets, HDAC2 was dispensable for HDAC1 binding to HDAC2-activated targets, supporting the notion of distinct classes of targets. Both active and repressed classes of gene targets demonstrated enhanced histone acetylation and methylation in HDAC2-null cells. Binding of the HDAC1/2-associated SIN3A corepressor was altered at most HDAC2-targets, but without a clear pattern. Overall, our study defines two classes of HDAC2 targets in human cells, with a dependence of HDAC1 on HDAC2 at one class of targets, and distinguishes unique functions for HDAC2

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Journal Article

Priyanka Somanath, ,, ,, McDonough, A., Ariza, J., ,, ,, Horton, K., and Knoepfler, P. S., “Behavior of Xeno-Transplanted Undifferentiated Human Induced Pluripotent Stem Cells Is Impacted by Microenvironment Without Evidence of Tumors.”, Stem Cells Dev, vol. 26, no. 19, 2017.[Abstract]

Human pluripotent stem cells (hPSC) have great clinical potential through the use of their differentiated progeny, a population in which there is some concern over risks of tumorigenicity or other unwanted cellular behavior due to residual hPSC. Preclinical studies using human stem cells are most often performed within a xenotransplant context. In this study, we sought to measure how undifferentiated hPSC behave following xenotransplant. We directly transplanted undifferentiated human induced pluripotent stem cells (hIPSC) and human embryonic stem cells (hESC) into the adult mouse brain ventricle and analyzed their fates. No tumors or precancerous lesions were present at more than one year after transplantation. This result differed with the tumorigenic capacity we observed after allotransplantation of mouse ESC into the mouse brain. A substantial population of cellular derivatives of undifferentiated hESC and hIPSC engrafted, survived, and migrated within the mouse brain parenchyma. Within brain structures, transplanted cell distribution followed a very specific pattern, suggesting the existence of distinct microenvironments that offer different degrees of permissibility for engraftment. Most of the transplanted hESC and hIPSC that developed into brain cells were NeuN+ neuronal cells, and no astrocytes were detected. Substantial cell and nuclear fusion occurred between host and transplanted cells, a phenomenon influenced by microenvironment. Overall, hIPSC appear to be largely functionally equivalent to hESC in vivo. Altogether, these data bring new insights into the behavior of stem cells without prior differentiation following xenotransplantation into the adult brain.

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NIRF 2017