Abstract
Understanding of pancreatic islet biology has greatly increased over the past few decades based in part on an increased understanding of the transcription factors that guide this process. One such transcription factor that has been increasingly tied to both β-cell development and the development of diabetes in humans is GLIS3. Genetic deletion of GLIS3 in mice and humans induces neonatal diabetes, while single nucleotide polymorphisms (SNPs) in GLIS3 have been associated with both Type 1 and Type 2 diabetes. As a significant progress has been made in understanding some of GLIS3’s roles in pancreas development and diabetes, we sought to compare current knowledge on GLIS3 within the pancreas to that of other islet enriched transcription factors. While GLIS3 appears to regulate similar genes and pathways to other transcription factors, its unique roles in β-cell development and maturation make it a key target for future studies and therapy.
Highlights
The pancreas serves a dual-function role within the body
Acinar cells produce and secrete enzymes involved in digestion through the pancreatic ductal network into the duodenum to aid in digestion, while pancreatic endocrine cells play a critical role in the regulation of glycemia via hormone secretion into the blood stream
With the exception of monogenic diabetes, where β-cell or pancreatic dysfunction is linked to mutations in one particular gene [3], diabetes mostly results from a combination of genetic and environmental factors
Summary
The pancreas serves a dual-function role within the body. Acinar cells produce and secrete enzymes involved in digestion through the pancreatic ductal network into the duodenum to aid in digestion, while pancreatic endocrine cells play a critical role in the regulation of glycemia via hormone secretion into the blood stream. We sought to review our current understanding of the GLIS3 gene as it relates to pancreas development, comparing as well as contrasting its role with that of other transcription factors prominent. We sought to review our current understanding of the GLIS3 gene2aosf i1t2 relates to pancreas development, comparing as well as contrasting its role with that of other transcription factors prominent in the field. We hope to highlight that while mice and humans lacking a functional copy of the GLIS3 gene display many phenotypes similar tionoththeefiretlrda.nWscerihpotipoentfoahctiogrhlkignhotckthoauttws, hthilee tmimicienagnadnhdufmeaatnusrelascokfinthgeapfuhnenctoiotynpael scodpifyfeorf itnhseuGbLtlIeS3bugtedneisdtiinsgpulaisyhmabalneywpahyesnforotympeosthsiemr itlraarntsocroitphteiorntrfaancstocrrisp, thioignhflaigcthotrinkgnGocLkIoSu3′tss, utnhieqtuime rinolgeainndpafenactrueraetsicodf ethveelpophmeneontty.pes differ in subtle but distinguishable ways from other transcription factors, highlighting GLIS3’s unique role in pancreatic development. This leads to unanswered questions of how GLIS3 protein is recruited to the promoter and regulatory regions of its target genes and how the distinct binding of these proteins to target genes is coordinated
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