Klf5 regulates muscle differentiation via directly targeted muscle-specific genes in cooperation with MyoD in mice

Deletion of Klf5 in satellite cells impaired muscle regeneration due to a failure of differentiation. Mechanistically, Klf5 controls transcription of muscle genes by interacting with MyoD and Mef2. These findings provide a potential intervention into the process of muscle regeneration through modulation of Klf5. Overall design: Genome wide localization of Transcription factors Klf5 and MyoD were assessed by ChIP-Seq. Genome-wide gene expression were analyzed by RNA-seq at indicated timepoint during myoblast differentiation.

卫星细胞（satellite cells）中Klf5的缺失会因分化障碍而损害肌肉再生。机制研究显示，Klf5可通过与MyoD及Mef2相互作用，调控肌肉相关基因的转录。上述发现为通过调控Klf5干预肌肉再生进程提供了潜在思路。
实验整体设计：通过染色质免疫共沉淀测序（ChIP-Seq）对转录因子Klf5与MyoD的全基因组定位情况进行了检测；在成肌细胞（myoblast）分化过程中的指定时间点，通过RNA测序（RNA-seq）对全基因组基因表达水平进行了分析。