Arjumand Ghazi, PhD

  • Associate Professor of Pediatrics

Arjumand Ghazi trained as a developmental biologist, completing her graduate studies in fly muscle development at the National Center for Biological Sciences, Tata Institute for Fundamental Research, India, and post-doctoral research in Cynthia Kenyon’s laboratory at the University of California, San Francisco (UCSF) on the genetics of aging in C. elegans. As a postdoc, she demonstrated that the proteasomal pathway of protein degradation regulates lifespan and identified genes and pathways that influence longevity based on signals from the reproductive system. She leads a research group that studies the molecular genetic pathways that link length of life (lifespan) with reproductive fitness, quality of aging (healthspan) and stress resistance mechanisms. Research from the Ghazi lab has shown that lifespan-promoting transcription factors coordinate fat production and breakdown to enhance longevity. Recently, the lab has discovered a novel role for one such factor, TCER-1, in having opposite impacts on lifespan and healthspan, and in repressing immune-resistance to divert cellular resources towards fertility.

She is committed to, and active in, graduate education and mentoring. She is the Associate Director of the Molecular Genetics and Developmental Biology (MGDB) graduate program, and a member of the Cell Biology and Molecular Physiology (CBMP) and Integrated Systems Biology (ISB) graduate programs. She is also an Associate Member of the University of Pittsburgh’s Aging Institute and Magee Women’s Research Institute, and has faculty appointments in the Departments of Developmental Biology and Cell Biology and Physiology.

Professional and Scientific Society Memberships:

  • Genetic Society of America, 2011-Present
  • Society for Developmental Biology, 2011-Present
  • Gerontological Society of America, 2018-Present

Education & Training

  • BS, Microbiology, Chemistry, Zoology, St. Ann's College, Osmania University, 1993
  • MS, Biotechnology, Hyderabad Central University, 1995
  • PhD, Developmental Biology / Molecular Genetics, National Centre for Biological Sciences, Tata Institute for Fundamental Research, 2001

Selected Publications

Keith SA, Amrit FRG, Ratnappan R and Ghazi A*. The C. elegans Healthspan and Stress-Response Assay Toolkit. Methods (2014). Aug 1;68(3):476-86. doi: 10.1016/j.ymeth.2014.04.003. PMID: 24727065

Amrit FRG, Steenkiste E, Ratnappan R, Chen SW, Kostka, D, McClendon B, Yanowitz J, Olsen CP and Ghazi A*. DAF-16 and TCER-1 facilitate adaptation to germline loss by restoring lipid homeostasis and repressing reproductive physiology in C. elegans. PLoS Genet. (2016). 10(12):e1005788. doi: 10.1371/journal.pgen.1005788. PMID: 26862916
Recommended by Faculty of 1000:

Keith SA, Maddux S, Zhong Y, Ferguson AA, Ghazi A and Alfred L. Fisher Graded proteasome dysfunction in C. elegans activates an adaptive response involving the conserved SKN-1 and ELT-2 transcription factors and the autophagy-lysosome pathway. PLoS Genet. (2016). 12(2):e1005823. doi: 10.1371/journal.pgen.1005823. PMID: 26828939.

McClendon TB, Rana M, Amrit FR, Fukushige T, Krause M, Ghazi A, Yanowitz JL*. X chromosome crossover formation and genome stability in Caenorhabditis elegans are independently regulated by xnd-1. G3: Genes, Genomes, Genetics. (2016). pii: g3.116.035725. doi: 10.1534/g3.116.035725. PMID: 27678523

Ratnappan R, Ward, JD, Yamamoto, KR and Ghazi A*. Nuclear hormone receptors as mediators of metabolic adaptability in response to reproductive perturbations. Worm (2016). 5(1): 1–12. PMID: 27073739

King CD, Singh D, Holden K, Govan AB, Keith SA, Ghazi A* and Robinson RASR*. Dataset of proteomics analysis of aging C. elegans exposed to Pseudomonas aeruginosa. Data in Brief (2017). 245-251.

Amrit FRG and Ghazi A*. Analysis of C. elegans transcriptomic data by the Tuxedo suite of the Galaxy pipeline. Journal of Visual Experimentation (JoVE) (2017). Apr 8;(122). doi: 10.3791/55473. PMID: 28448031

King CD, Singh D, Holden K, Govan AB, Keith SA, Ghazi A* and Robinson RASR*. Proteomic Identification of Virulence-Related Factors in Young and aging C. elegans exposed to Pseudomonas aeruginosa. Journal of Proteomics (2018). 2018 Apr 12. pii: S1874-3919(18)30165-9. doi: 10.1016/j.jprot.2018.04.006. PMID: 29656019

Amrit FRG, Naim N, Ratnappan R, Loose, JA, Mason C, Steenberge L, McClendon TB, Wang G, Driscoll M, Yanowitz JL and Ghazi A*. The longevity-promoting factor, TCER-1, widely represses stress resistance and innate immunity. Nature Communications (2019). 10, 3042. DOI PMID: 31316054.

Full Publication List via NIH PubMed »

Academic and Research Interests

  • Aging
  • Reproduction
  • Metabolism
  • Lipid
  • C. Elegans
  • Healthspan
  • Longevity
  • Proteostasis
  • Lifespan
  • Development
  • Germline

Research Grants

NIH 1R01AG051659-01A1, The coordination of lipid production and breakdown in metabolism and aging (PI), $1,246,600

NIH 1R01AG051659-01A1 Administrative Supplement, The coordination of lipid production and breakdown in metabolism and aging (PI), $64,478

NIH 1R01AG051659-01A1, Administrative Supplement, The role of systemic regulation of lipid anabolism and catabolism on C. elegans models of Abeta toxicity (PI), $303,796