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Transcriptome analysis of E15.5 wild-type (Tbr2-f/+) andTbr2-Isl1/+ retinae

ABSTRACT: Isl1 encodes a member of the LIM/homeodomain family of transcription factors. During retinal development. Isl1 plays a critical role in RGC fate specification. Tbr2 is essential for the formation and maintaining the survival of ipRGCs. In this study, we tested whether ectopically expressing Isl1 in Tbr2-expressing cells affects the developmental program of Tbr2-expressing retinal neurons, including ipRGCs and a subset of wide-field displaced amacrine cells. We generated a Tbr2-Isl1 knock-in allele using gene targeting technique, and then used RNA-seq approach to compare transcriptome profiles between E15.5 wild-type (Tbr2-flox/+) and Tbr2-Isl1/+ retinas to uncover how Isl1 affects Tbr2-regulated genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE149791 | GEO | 2025/04/30

REPOSITORIES: GEO

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Project description:Visceral fat (VF) and subcutaneous fat (SF) are developmentally different tissues with different gene expression. Islet-1 (ISL1), a LIM-homeobox transcription factor with important developmental and regulatory function in islet, neural, and cardiac tissue, is virtually absent in SF but substantially expressed in the stromovascular [preadipocyte containing] fraction of VF; expression correlates negatively with adiposity in rodents and man. ISL1 expression is transiently increased in 3T3-L1 preadipocytes during early differentiation, suggesting a functional role. To examine the role of ISL1 in adipogenesis, we tested whether retroviral overexpression of ISL1 in 3T3-L1 preadipocytes affected their ability to differentiate into mature adipocytes. Terminal differentiation was assessed by Oil Red O [lipid droplet] staining and by immunoblot detection of adipocyte marker proteins, including aP2 and GLUT4. ISL1 significantly inhibited lipid droplet formation, reduced lipid accumulation (about 80% inhibition, p<0.05), and substantially inhibited aP2 and GLUT4 expression. ISL1 did not inhibit expression of C/EBPb and C/EBPd after induction of differentiation, but reduced PPARg and C/EBPa by >50% at both mRNA and protein level. In addition, the PPARg agonist, rosiglitazone, substantially rescued ISL1 inhibited adipogenesis in the absence of exogenous PPARg, and fully rescued in the presence of exogenous PPARg. In summary, ISL1 overexpression inhibited fat droplet formation, lipid accumulation, and adipocyte-specific gene expression; there was accompanying inhibition of C/EBPa, PPARg and downstream gene expression. We conclude that ISL1 overexpression inhibited adipocyte differentiation by inhibition of PPARg regulated gene expression. As abdominal obesity strongly correlates with insulin resistance, and cardiovascular risk, ISL1 up-regulation may impact abdominal obesity and its concomitant metabolic derangements. Total cellular RNA was isolated from 3T3-L1 cells expressing Flag-ISL1 or not at 48 h following treatment with differentiation cocktail. Individual RNA from biological triplicates was used for microarray analysis.

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Transcriptome analysis of E15.5 wild-type (Tbr2-f/+) andTbr2-Isl1/+ retinae

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