Bio


I am a PhD student in Stanford Biosciences, department of Molecular and Cellular Physiology. I am broadly interested in basic molecular processes that occur in the cell and aim to delineate these mechanisms using biochemistry, molecular biology, bioinformatics and biophysics. I am also available as a consultant for bio-tech ventures.

Academic Appointments


Honors & Awards


  • Knight-Hennessy Fellowship, Stanford University (2019-2025)
  • Stanford Graduate Fellowship, Stanford University (2019-2025)
  • Graduate Research Fellowship Program, National Science Foundation (2019-2025)
  • Winston Churchill Scholarship, Churchill Foundation (2018)
  • Summa Cum Laude (4.0), University of Maryland, College Park (2018)
  • Dean's List, University of Maryland, College Park (2014-2018)
  • Integrated Life Sciences Honors Citation, University of Maryland, College Park (2016)
  • J. Howard Brown Award, American Society for Microbiology (2018)
  • University Medal Finalist, University of Maryland, College Park (2018)
  • HHMI Undergraduate Research Fellowship, Howard Hughes Medical Institute/University of Maryland, College Park (2017,2018)
  • Barry M. Goldwater Scholarship, Goldwater Foundation (2016)
  • Dr. Laffer Award for Excellence in Research, University of Maryland, College Park (2016)
  • Maryland Summer Scholars Fellowship, University of Maryland, College Park (2015,2016)
  • Banneker/Key Scholarship, University of Maryland, College Park (2014)

Professional Education


  • MPhil, University of Cambridge, Biology (Pathology) (2019)
  • BSc, University of Maryland, College Park, Molecular and Cellular Physiology (2018)

All Publications


  • Evidence for a novel overlapping coding sequence in POLG initiated at a CUG start codon. BMC genetics Khan, Y. A., Jungreis, I. n., Wright, J. C., Mudge, J. M., Choudhary, J. S., Firth, A. E., Kellis, M. n. 2020; 21 (1): 25

    Abstract

    POLG, located on nuclear chromosome 15, encodes the DNA polymerase γ(Pol γ). Pol γ is responsible for the replication and repair of mitochondrial DNA (mtDNA). Pol γ is the only DNA polymerase found in mitochondria for most animal cells. Mutations in POLG are the most common single-gene cause of diseases of mitochondria and have been mapped over the coding region of the POLG ORF.Using PhyloCSF to survey alternative reading frames, we found a conserved coding signature in an alternative frame in exons 2 and 3 of POLG, herein referred to as ORF-Y that arose de novo in placental mammals. Using the synplot2 program, synonymous site conservation was found among mammals in the region of the POLG ORF that is overlapped by ORF-Y. Ribosome profiling data revealed that ORF-Y is translated and that initiation likely occurs at a CUG codon. Inspection of an alignment of mammalian sequences containing ORF-Y revealed that the CUG codon has a strong initiation context and that a well-conserved predicted RNA stem-loop begins 14 nucleotides downstream. Such features are associated with enhanced initiation at near-cognate non-AUG codons. Reanalysis of the Kim et al. (2014) draft human proteome dataset yielded two unique peptides that map unambiguously to ORF-Y. An additional conserved uORF, herein referred to as ORF-Z, was also found in exon 2 of POLG. Lastly, we surveyed Clinvar variants that are synonymous with respect to the POLG ORF and found that most of these variants cause amino acid changes in ORF-Y or ORF-Z.We provide evidence for a novel coding sequence, ORF-Y, that overlaps the POLG ORF. Ribosome profiling and mass spectrometry data show that ORF-Y is expressed. PhyloCSF and synplot2 analysis show that ORF-Y is subject to strong purifying selection. An abundance of disease-correlated mutations that map to exons 2 and 3 of POLG but also affect ORF-Y provides potential clinical significance to this finding.

    View details for DOI 10.1186/s12863-020-0828-7

    View details for PubMedID 32138667