A modular enhancer mediates SCRT2 repression of ISLET1 in the spinal cord

模块化增强子介导脊髓中SCRT2对ISLET1的抑制

阅读:2

Abstract

How transcriptional programs coordinate the transition from neural progenitors to lineage-committed neurons in the spinal cord remains poorly understood. While much is known about transcription factors acting in the proliferative and differentiated zones, the role of intermediate zone (IZ) factors during lineage specification is less clear. Here, we investigate the function of SCRATCH2 (SCRT2), expressed in the postmitotic cells of the IZ, during dorsal interneuron differentiation. Overexpression of SCRT2 in vivo reduced the number of ISLET1+ dorsal interneurons. Chromatin profiling revealed that SCRT2 primarily binds to intergenic, transcriptionally inactive regions near neurogenic genes. Among these, we identified a conserved regulatory element, ECR4, located between ISLET1 and PARP8. Functional assays showed that ECR4 drives neural transcription and is composed of two subregions: ECR4B, an enhancer activated by ISLET1 and POU4F1, and ECR4A, which contains SCRT2 binding motifs and mediates transcriptional repression. Mutation of the vCES-box, a predicted SCRT2-binding motif within ECR4A, abolished repression, confirming a repressive regulatory interaction. Together, these data support a model in which SCRT2 represses ISLET1 through ECR4 to modulate dI3 lineage specification. These findings identify a novel regulatory mechanism linking intermediate zone transcriptional repression to dorsal interneuron development in the spinal cord.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。