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UID:1191@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20230905T130000

DTEND;TZID=Asia/Jerusalem:20230905T133000

DTSTAMP:20230903T085708Z

URL:https://biology.technion.ac.il/en/seminars/msc-graduate-seminar-roy-gu
 rwicz/

SUMMARY:Msc Graduate Seminar-Roy Gurwicz [No Categories]
DESCRIPTION:Location: Faculty Of Biology Auditorium/ZOOM: https://technion.
 zoom.us/j/97039787933  Roy Gurwicz\n Affiliation: \n Host:Dr. Sharon Nadav
 \n Identification of molecules which control in-vitro progenitor to endocr
 ine cell differentiation of hESCs-derived pancreatic cells\n\n\nType 1 dia
 betes is a chronic disease\, caused by the loss of insulin-producing β-ce
 lls which reside in the pancreatic islets of Langerhans. In-vitro differen
 tiation of human embryonic stem cells into β-cells could serve as a trans
 plantation source\, but the high cost and low yield of current protocols m
 ake this promising therapy unaffordable for most patients. Although endocr
 ine cells rarely divide\, in-vitro differentiation includes an intermediat
 e progenitor cell-state which\, if maintained\, could serve to expand the 
 differentiating-cells' number\, and reduce costs.\nTo identify factors whi
 ch control the progenitor-endocrine balance\, we performed a high throughp
 ut screen using RNA-sequencing Of Selected Amplicons (ROSA-HTS) which allo
 ws targeted sequencing of hundreds of genes from thousands of samples. Of 
 1280 molecules\, we performed full RNA-sequencing on 89 “hits”\, and d
 iscovered novel effector molecules that shift progenitor-to-endocrine bala
 nce. Among these\, we discovered acetylcholine-receptor effectors (Nicotin
 ic agonist and Muscarinic antagonist) which induced progenitor gene-expres
 sion\, whereas PI3K\, AKT or mTOR inhibition induced an early endocrine st
 ate. In addition\, we discovered novel molecular pathways which were not d
 irectly targeted by the screen\, but whose mediated regulation uncovers a 
 potential influence on pancreatic differentiation. For instance\, Interfer
 on-I inhibition seems to induce endocrine state\, whereas Interleukins 2 a
 nd 18 activation seems to induce progenitor state.\nAchieving the optimal 
 combination of molecules which effect the progenitor-to endocrine balance 
 is expected to have a synergic effect\, and thus increase yield of existin
 g protocols for β-cell differentiation.\n\n\n\n 
LOCATION:Faculty Of Biology Auditorium/ZOOM: https://technion.zoom.us/j/970
 39787933

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