Xiao-Dun Yang, Graduate Student
Gu and Wright Labs







Record History
Added on December 4, 2018 at 2:19 PM by Uttz, Pam
Modified on April 5, 2019 at 1:09 PM by Uttz, Pam
Shared with (contributions)
Public: SPRING Meeting

Meeting Details

Start Date / Time April 10, 2019 at 9:00 AM
End Date / Time April 10, 2019 at 10:00 AM
Duration 1 hour(s)
Location 9455 MRB IV
Presenter Name Xiao-Dun Yang
Presentation Title “The roles of Sin3A co-regulator in endocrine progenitor and differentiated islet cells”
Status This meeting has already occurred

Meeting Agenda/Notes

The previous data from the Gu lab showed that Myt factors (myelin transcription factors) regulated islet-cell differentiation and tuned beta-cell stress responses. However, it is not clear what co-regulators may be recruited by Myt factors to regulate the expression of cell fate genes or stress genes in beta cells. Sin3A (SWI-independent-3A) is a transcriptional co-regulator that interacts with transcription factors (TFs) to recruit chromatin-modifying enzymes to regulate target gene transcription. Sin3A has been shown to associate with Myt factors in large protein complexes in pancreatic beta cells. The interaction between Sin3A and Myt factors is also supported by the evidence that in neuronal cells, the Sin3A close paralog, Sin3B, directly interacts with Myt factors to repress target gene expression. This study focuses on how Sin3A regulates beta-cell differentiation, function, and survival at least partly by interacting with Myt factors. I have inactivated Sin3A in the pancreatic endocrine progenitors and pancreatic progenitors using Ngn3-Cre and Pdx1-Cre, respectively. I will present the phenotypes of the Sin3A-knockout mice and the cellular and molecular mechanisms of these phenotypes. My data indicate that Sin3A is not required for beta-cell differentiation during embryogenesis but is required for postnatal beta-cell function and survival at least partly by tuning the stress responses. This study may indicate a novel mechanism of how beta cells regulate the stress responses within proper levels to maintain normal function and survival, which might provide new clues to treat cellular stress-induced loss of functional beta-cell mass in diabetes.


Document Spring_2019_Email_Notice_Yang.pdf - Added on April 5, 2019 at 1:09 PM by Pam Uttz