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UID:1221@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20240507T130000

DTEND;TZID=Asia/Jerusalem:20240507T140000

DTSTAMP:20240502T094307Z

URL:https://biology.technion.ac.il/en/seminars/phd-graduate-seminar-akmara
 l-rakhymzhanova/

SUMMARY:PhD Graduate Seminar- Akmaral Rakhymzhanova [No Categories]
DESCRIPTION:Location: Hybrid- in the Faculty Auditorium/ZOOM: https://techn
 ion.zoom.us/j/99062456099   Akmaral Rakhymzhanova\n Affiliation: \n Host:D
 r. Noga Ron-Harel \n Alanine – a metabolic liability ‘by choice’\n\n
 Abstract:\n\nT lymphocytes\, the cellular arm of the adaptive immune syste
 m\, maintain host homeostasis and orchestrate an immune response to pathog
 ens and internal threats like tumors and injuries. Upon encountering their
  cognate antigen\, T cells enter a phase of rapid cell growth expansion. T
 his transition from quiescence to active growth is driven by the reprogram
 ming of cellular metabolism\, transitioning from low-rate catabolism to ma
 ssive biosynthesis. Success in this transformation relies on the microenvi
 ronment providing essential fuels such as glucose and amino acids. Our pre
 vious work highlighted T cell dependence of extracellular alanine pools fo
 r activation\, showing that T cells do not express GPT (Glutamate Pyruvate
  Transaminase)\, an alanine synthesizing enzyme.  As a result\, alanine d
 eprivation inhibited protein synthesis and arrested T cell activation. An 
 intriguing question arose: Why do T cells ‘choose’ this metabolic liab
 ility?\n\nWe hypothesized that T cells purposefully suppress GPT expressio
 n to enable pyruvate flux into other metabolic pathways. In this study\, w
 e tested this hypothesis by overexpressing GPT in primary T cells and exam
 ining its effect on T cell metabolism and function. GPT overexpression res
 cued T cell growth\, activation\, and proliferation under conditions of al
 anine deprivation\, albeit with a concomitant decrease in cell viability. 
 Untargeted metabolomics highlighted significant alterations in metabolism 
 driven by GPT overexpression\, with lower carbon flux into the mitochondri
 a\, reduced cellular pools of aspartate and nucleotides\, and accumulation
  of 2-hydroxyglutarate (2-HG).  Intriguingly\, these robust changes in me
 tabolism did not affect proliferation but compromised cell viability.\n\nO
 ur findings shed light on T cells fuel portioning and the consequences of 
 its interruption. 
LOCATION:Hybrid- in the Faculty Auditorium/ZOOM: https://technion.zoom.us/j
 /99062456099

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