Bod1l, also known as Borealin-like, plays crucial roles in multiple biological processes. It is involved in pathways related to chromatin regulation, DNA replication fork protection, and is associated with the maintenance of genome stability. Its functions are essential for normal cell development and are linked to various disease-related processes [1-5].

In terms of chromatin regulation, Bod1l knockout reduces leukemia cells both in vitro and in vivo, mimicking the transcriptional profiles of SETD1A knockout cells. It mediates the chromatin binding of H3K4 methyltransferase SETD1A. Loss of Bod1l reduces SETD1A distribution at transcriptional start sites, induces transcriptional elongation defect, and increases RNA polymerase II content at TSS, yet does not reduce H3K4me3 [1].

In DNA replication fork protection, Bod1l-deficient cells show exquisite sensitivity to replication stress and uncontrolled resection of damaged replication forks due to failure to stabilize RAD51 at these forks. Blocking DNA2-dependent resection or down-regulating helicases BLM and FBH1 can suppress catastrophic fork processing and chromosomal damage in these cells [2].

In conclusion, Bod1l is a key factor in chromatin-associated transcriptional regulation and replication fork protection, safeguarding genome stability. Studies using gene knockout models have revealed its significance in leukemia and the potential implications in diseases related to replication stress and genome instability, providing valuable insights into the underlying molecular mechanisms and potential therapeutic targets [1,2].