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Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [H3K27me3 CUT&RUN E14.5 and P0]

ABSTRACT: Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.

ORGANISM(S): Mus musculus

PROVIDER: GSE202728 | GEO | 2023/02/15

REPOSITORIES: GEO

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Project description:The early retinal progenitor-expressed gene Sox11 regulates the timing of the differentiation of retinal cells. Sry-related HMG box (Sox) proteins play diverse and critical roles in a variety of morphogenetic processes during embryonic development. Sox11 and Sox4 are members of the SoxC subtype, and we found that Sox11 was strongly expressed in early retinal progenitor cells, and that when expression of Sox11 subsided around birth, Sox4 expression began. To analyze the role of Sox11 and Sox4 in retinal development, we perturbed their expression pattern by expressing them ectopically in retinal explant culture. Overexpression of Sox11 or Sox4 in retinal progenitors resulted in similar phenotypes, that is, increased cone cells and decreased Muller glia. Sox11-knockout retinas showed delayed onset and progress of differentiation of early-born retinal cells during the embryonic period. After birth, retinal differentiation took place relatively normally, probably because of the redundant activity of Sox4, which starts to differentiate around birth. Neither overexpression nor loss-of-function analysis gave any evidence that Sox11 and Sox4 directly regulate transcription of genes critical to early-born retinal cells. However, histone H3 acetylation status of the early neurogenic genes was lowered in knockout retinas, suggesting that Sox11 regulates the timing of differentiation in early-born retinas by creating an epigenetic state that helps to establish the competency to differentiate. We also found that the unique expression patterns of Sox11 and Sox4 may be achieved by the Notch signaling pathway and by epigenetic regulation. Taking our findings together, we propose that the precise regulation of Sox11 and Sox4 expression during retinogenesis by multiple mechanisms leads to the fine adjustment of retinal differentiation. To delineate the molecular mechanisms underlying the retinal action of Sox11, we performed microarray analysis of E18 retinas from wild-type and Sox11 knockout mice. Total RNA was obtained from each one retina of Sox11 knockout and wild-type littermate embryos at E18.

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Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [H3K27me3 CUT&RUN E14.5 and P0]

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