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PRODID:-//NCBS Banglaore//NONSGML NCBS Hippo//EN
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TZID:Asia/Bengaluru
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TZOFFSETFROM:+0530
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DTSTART:19700101T000000
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BEGIN:VEVENT
UID:20260412T161256-13035.1-hippo.ncbs.res.in
DTSTAMP:20260412T161256
ORGANIZER;CN:Zeenat Rashida:MAILTO:rzeenat@instem.res.in
DTSTART;TZID=Asia/Bengaluru:20211122T113000
DTEND;TZID=Asia/Bengaluru:20211122T123000
SUMMARY:Thesis Seminar by Ms Zeenat Rashida on 'Roles of Kog1/Raptor in maintaining metabolic homeostasis under fluctuating nutrient environments'
DESCRIPTION:<p class="ql-align-justify">For efficient cell growth, integration of external nutrient inputs by various signalling pathways into metabolic outputs is crucial. In a eukaryotic cell, the TORC1 and AMPK/SNF1 signalling pathways are two such conserved pathways with important roles in maintaining metabolic homeostasis and growth. Typically, TORC1 and AMPK/SNF1 function in contrasting manner. TORC1 is active under nutrient rich conditions, whereas the AMPK/SNF1 activity is required under nutrient limitation. Much less is known about AMPK/SNF1 activity under rich nutrient condition. Similarly, the functions of TORC1 or its components under glucose and amino acid limitation are relatively unknown. Using the model eukaryote <em>Saccharomyces cerevisiae</em>, we have identified a mutant of Kog1/Raptor - an essential component of TORC1, which revealed a specific growth defect exclusively under glucose and amino acid limitation, where TORC1 kinase activity is undetectable. Combining metabolic flux and comparative transcriptome analysis, we find this growth defect is due to delayed metabolic rewiring under nutrient limitation. This results in an imbalance in the routing of carbon flux towards amino acid biosynthesis and gluconeogenesis. Since gluconeogenesis is primarily controlled by AMPK/SNF1, examining SNF1 activity revealed altered phosphorylation status of the primary SNF1 targets - Mig1 and Cat8, suggesting Kog1 dependent control of SNF1 activity. This Kog1 dependent SNF1 regulation occurs even under rich nutrient condition and is rapamycin/TORC1 kinase independent. Notably, activating SNF1 in the mutant Kog1 cells, leads to rescue of the growth defect observed under nutrient limitation. Collectively, we discover a novel mechanism of Kog1 dependent activation of SNF1. This enables effective glucose derepression and gluconeogenesis activation under nutrient limitation. This also allows cells to appropriately allocate carbon flux towards amino acid biosynthesis, irrespective of glucose availability, in order to maintain metabolic homeostasis.</p><p class="ql-align-justify">&nbsp;</p><p class="ql-align-justify">Reference:</p><p><span style="color: rgb(34, 34, 34);">Rashida, Z., Srinivasan, R., Cyanam, M. and Laxman, S., 2021. Kog1/Raptor mediates metabolic rewiring during nutrient limitation by controlling SNF1/AMPK activity.&nbsp;</span><em style="color: rgb(34, 34, 34);">Science Advances</em><span style="color: rgb(34, 34, 34);">,&nbsp;</span><em style="color: rgb(34, 34, 34);">7</em><span style="color: rgb(34, 34, 34);">(16), p.eabe5544.</span></p>
LOCATION:Remote Video Conference
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