Sheetal Gandotra is interested in understanding mechanisms whereby M. tuberculosis (Mtb) is able to adapt to different metabolic niches. She uses a combination of genetics and cell biology to understand mycobacterial survival strategies under extremes of nutrient availability. She is also interested in understanding how host cell metabolism is altered during infection and identifying pathways that can be manipulated in order to deregulate these adaptive pathways in Mtb.
Her major interests are:
Understanding metabolic plasticity of mycobacteria in different models of infection
Developing novel fluorescence based tools for studying mycobacteria-host interaction
- Human frame shift mutations affecting the carboxyl terminus of perilipin increase lipolysis by failing to sequester the adipose triglyceride lipase (ATGL) coactivator AB-hydrolase-containing 5 (ABHD5). Gandotra S, Lim K, Girousse A, Saudek V, O'Rahilly S, Savage DB. J Biol Chem. 2011. 286(40):34998-5006.
- Perilipin Deficiency and Autosomal Dominant Partial Lipodystrophy. Gandotra S, Le Dour C, Bottomley W, Cervera P, Giral P, Reznik Y, Charpentier G, Auclair M, Delépine M, Barroso I, Semple RK, Lathrop M, Lascols O, Capeau J, O’Rahilly S, Magré J, Savage DB, Vigouroux C. New England Journal of Medicine. 2011. 364(8):740-8.
- The Mycobacterium tuberculosis proteasome active site threonine is essential for persistence in vitro and in mice yet dispensable for replication and resistance to nitric oxide. Gandotra S, Lebron M, Ehrt S. PLOS Pathogens. 2010. 6(8). pii: e1001040.
- In vivo gene silencing identifies the Mycobacterium tuberculosis proteasome as essential for the bacteria to persist in mice. Gandotra S, Schnappinger D, Monteleone M, Hillen W, Ehrt S. Nature Medicine. 2007. 13(12):1515-1520.
- Nucleotide-Binding Oligomerization Domain Protein 2-Defficient mice control infection with Mycobacterium tuberculosis. Gandotra S, Jang S, Murray PJ, Salgame P, Ehrt S. Infection & Immunity. 2007. 75(11):5127-5134.