Priyanka Verma, Ph.D.

Assistant Professor
Internal Medicine
Oncology

Cancer Biology Program
Molecular Cell Biology Program
Molecular Genetics and Genomics Program
Biochemistry, Biophysics, and Structural Biology Program

  • 314-286-1906

  • 314-286-1916

  • McDSci 840

  • vermap@wustl.edu

  • https://www.vermalab.org/

  • https://twitter.com/priyanka13verma

  • DNA repair and replication; Genomic instability in cancers; Oncogenes; BRCA-mutation

  • Understanding DNA repair mechanisms that impact cancer etiology and responses to chemotherapies

Research Abstract:

With an overarching goal to understand the causes and consequences of DNA damage in cancers, research in my lab aims to answer the following questions:

What dictates cellular responses to chemotherapies that target DNA repair pathways?
DNA repair pathways have been the target of multiple FDA-approved and experimental chemotherapies. The success of these therapies depends on the increased reliance of rapidly proliferating cancer cells on DNA replication and repair pathways. However, holistic responses to chemotherapies are an amalgamation of multiple cellular pathways and physiological settings. We are interested in decoding the molecular determinants that dictate chemotherapeutic response with the broad goal of tailoring treatment regimens and uncovering biological circuits that ensure genomic stability.

How cancer cells deal with roadblocks to replication?
Oncogenic transformations are often associated with genomic alterations that can challenge DNA replication. Owing to the essentiality of genome duplication for cell survival, cancers evolve pathways to surmount obstacles to replication. Intriguingly, depending on the cellular context, these obstacles come in “different flavors”. By designing genetically defined systems to mimic different replication stress responses, the lab aims to define genome rescue mechanisms that are common and unique across cancer types.

What are the endogenous DNA lesions in BRCA-mutant cancer cells?
Cancers are characterized by aberrations in chromosomal numbers and characteristic DNA lesions, including damaged replication forks, single-strand breaks and double-strand breaks. The endogenous sources of these abnormalities remain unclear. In theory, any unresolved chemical modification in the nucleotide backbone of DNA can be the initiating molecular event for genomic instability when HR fails. We are interested in examining the unexplored link between nucleotide abnormalities and oncogenic transformations in HR-deficient cancers. These findings can be the key to understanding the innate molecular events that led to malignancy, and perhaps also reveal the basis for the known predilection of HR deficiency to result in cancers only in specific tissue types. This information can result in the discovery of biomarkers that can aid in the early detection of cancer. It may also be used to avoid exogenous exposures that lead to the genesis of such precipitating lesions.

We employ advanced CRISPR genetic screens and cancer genome mining tools to uncover biological circuits that are essential in cells with compromised DNA repair. This information is then combined with several biochemical and cellular tools to decode the mechanisms and consequences of these cancer-specific re-wiring events.

Mentorship and Commitment to Diversity Statement:
As a mentor, I am committed to ensure that my mentees receive the best training and experiences vital for a successful career trajectory. I aim to do so by creating a positive, stimulating and helpful lab environment. An environment where every suggestion is heard, and every opinion is respected. I aspire to help my mentees further their skills in formulating innovative hypothesis, critically assessing research, practicing best and rigorous scientific approaches and above all enjoy the process of making discoveries!

I am committed to creating a research environment where people of all backgrounds can feel comfortable, respected, and equally engaged. My efforts are guided by my own personal experiences and those of my past mentees, which have taught me that privilege can often be blinding, and it is instrumental to bring awareness towards gender and racial inequality. I believe that holding honest and in-depth conversations about diversity and discrimination in a public platform can not only help bring awareness on these issues but also aid in generating a sense of comfort and trust in my relationship with my mentees. I strive to put my best efforts in fostering a diverse, inclusive and equitable scientific community. After all, the thrill and satisfaction of scientific discovery should not be restricted to a few!

Selected Publications:

Verma P.*, Greenberg RA*. Communication between chromatin and homologous recombination. Curr. Opin. Genet. Dev., 71, 1-9,2021. (*Corresponding authors)

Verma P., Zhou Y., Cao Z., Deraska P., Arai E., Deb M., Li W., Li Y., Patankar S., Faryabi RB., Shi J., Greenberg RA. ALC1 and PARP activities coordinate chromatin accessibility and viability in homologous recombination deficient cells. Nat Cell Biol., 23(2),160-171,2021.

Verma P., Dilley RL, Zhang T, Gyparaki MT, Li Y, Greenberg RA. RAD52 and SLX4 act nonepistatically to ensure telomere stability during alternative telomere lengthening. Genes Dev. 33, 221-235, 2019.

Verma P.*, Dilley RL.*, Gyparaki MT., Greenberg RA. Direct Quantitative Monitoring of Homology-Directed DNA Repair of Damaged Telomeres. Methods in enzymology. 600, 107-134, 2018. (*Equal first author)

Dilley RL., Verma P., Cho NM., Winters HD., Wondisford A., Greenberg RA. Break-induced telomere synthesis underlies homology-directed telomere maintenance. Nature. 539, 54-58, 2016.

Verma P., Greenberg RA. Non-canonical views of homology directed DNA repair. Genes Dev. 30,1138-1154, 2016.

Kleiner RE., Verma P., Molloy KR., Chait BT., Kapoor TM. A chemical proteomics approach reveals a direct interaction between 53BP1 and ϒH2AX involved in the DNA damage response. Nat. Chem. Biol. 11, 807-814, 2015.

Anand A.*, Verma P.*, Singh AK., Kaushik S., Pandey R., Shi C., Kaur H., Chawla M., Elechalawar CK., Kumar D., Yang Y., Bhavesh NS., Banerjee R., Dash D., Singh A., Natrajan VT, Ojha AK., Aldrich CC., Gokhale RS. Polyketide quinones are alternate intermediate electron carriers during mycobacterial respiration in oxygen-deficient niches. Mol. Cell. 60, 637-650, 2015. (*Equal first author)

Goyal A.*, Verma P.*, Ananadkrishna M., Gokhale RS., Sankaranarayanan R. Molecular basis of the functional divergence of Fatty Acyl-AMP Ligase biosynthetic enzymes of Mycobacterium tuberculosis. J. Mol. Biol. 416, 221-238, 2012. (*Equal first author) (Cover Page Article)

Kim H., Xu H., George E., Hallberg D., Kumar S., Jagannathan V., Medvedev S., Kinose Y., Devins K., Verma P., Ly K., Wang Y., Greenberg RA., Schwartz L., Johnson N., Scharpf, RB., Mills GB., Zhang R., Velculescu VE., Brown EJ., Simpkins, F. Combination PARP and ATR inhibition causes complete and durable responses in PARP inhibitor and platinum resistant ovarian cancer. Nat Commun. 11(1),1-16 ,2020.

Pamula MC., Carlini L., Forth S., Verma P., Suresh S., Legant W., Betzig E., and Kapoor TM. High-resolution imaging reveals how the spindle midzone impacts chromosome movement. J Cell Biol. 218(8), 2529-2544, 2019.

Resmi MS., Verma P., Gokhale RS., Soniya EV. Identification and characterization of a Type III Polyketide synthase involved in quinolone alkaloid biosynthesis from Aegle marmelos Correa. J. Biol. Chem. 288, 7271-7281, 2013.

Singh V., Jamwal S., Jain R., Verma P., Gokhale R., Rao KV. Mycobacterium tuberculosis-driven targeted recalibration of macrophage lipid homeostasis promotes the foamy phenotype. Cell Host Microbe. 12, 669-681, 2012.

Swaroop PS., Raut G., Gonnade RG., Verma P., Gokhale RS., Reddy DS. Anti-tuberculosis Agent Diaportheone B: Synthesis, absolute configuration, assignment and anti-TB activity of its analogues. Org. Biomol. Chem. 10, 5385-5394, 2012.

Raut N.G., Chakraborty K., Verma P., Gokhale RS., Reddy DS. Synthesis of isomeric corniculatolides. Tetrahedron Lett. 53, 6343-6346, 2012.

Arora P., Goyal A., Natarajan VT., Rajakumara E., Verma P., Gupta R., Yousuf M.,Trivedi OA., Mohanty D., Tyagi A., Sankaranarayanan R., Gokhale RS. Mechanistic and functional insights into fatty acid activation in Mycobacterium tuberculosis. Nat. Chem. Biol. 5, 166-173, 2009.


Last Updated: 10/17/2021 8:46:14 PM

Back To Top

Follow us: