A blueprint to understand cohesin

Acute myeloid leukemia (AML) is a heterogenous hematopoietic malignancy that arises from clonal expansion and abnormal differentiation of myeloid precursor cells. Recently, recurrent mutation of cohesin complex has been discovered in AML based on next generation sequencing. Cohesin complex mainly functions as maintaining sister chromatid cohesion during mitosis, which also plays a prominent role in gene expression. Cohesin mutations confer both enhanced self-renewal and altered differtiation to hematopoietic stem and progenitor cells. Of note, cohesin mutations are associated with Down syndrome-associated acute megakaryocytic leukemia (DS-AMKL). Cohesin mutation provides potential target for clinical AML treatment. In this paper, the pathogenesis and progress of cohesin mutation in AML are reviewed. Key words: Leukemia, myeloid, acute; Mutation; Cohesin; Down syndrome-associated acute megakaryocytic leukemia (DS-AMKL)

Genome organization: Compartmentalizing chromatin without cohesin.

During the past ten years, genome-wide analysis of genetic alterations in myelodysplastic syndromes (MDS) has improved our understanding of their pathogenesis. Especially, single nucleotide polymorphism array karyotyping and next-generation sequencing technologies (NGS) have unveiled frequent genetic changes in novel functional pathways, including DNA methylation, RNA splicing and cohesin complex formation, in MDS. Moreover, NGS shed light on the clonal evolution which occurs during the development and progression of MDS, pre-cancerous lesions of MDS, and the effects of germline mutations in MDS.

Chromosome biology: In and out through the same cohesin door.

Cohesin mediates DSB-independent homolog pairing during meiosis

Cohesin Does the Business

From the XXVII North American Testis Workshop: the function of SMC and other cohesin proteins in meiosis.