Functional antagonism of the Polycomb-Group genes eed and Bmi1 in hemopoietic cell proliferation

Article Abstract:

Evidence for functional antagonism of the mouse Polycomb-Group (PcG) genes eed and Bmi1 in hemopoietic cell proliferation is discussed. Heterozygosity for an eed-null allele brings on clear myelo- and lymphoproliferative defects. Thus eed acts in the negative regulation of the pool size of myeloid and lymphoid progenitor cells. Intercross experiments with eed and Bmi1 mutant mice show that Bmi1 is epistatic to eed in control of primitive bone marrow cell proliferation. It appears that hemopoietic cell proliferation is regulated by relative contributions of repressive and enhancing PcG gene complexes, that is Eed- and Bmi1-containing ones, respectively.

Canada, Netherlands, Statistical Data Included, Genetic aspects, Mice, Mice (Rodents), Cytochemistry, Cell proliferation, Hematopoietic system

A Brg1 mutation that uncouples ATPase activity from chromatin remodeling reveals an essential role for SWI/SNF-related complexes in beta-globin expression and erythroid development

Article Abstract:

The Brg1 catalytic subunit of SWI/SNF-related complexes has been implicated in; many developmental and physiological processes, but null homozygoes die as blastocysts prior to implantation. To circumvent this early embryonic lethality, an ENU mutagenesis screen was performed and generated a Brg1 hypomorph mutation in the ATPase domain and it was revealed that Brg1 is the first chromatin-modifying factor shown to be required for beta-globin regulation and erythropoiesis in vivo.

Chromatin, Adenosine triphosphatase, Beta globulins, ATPases

Maternal BRG1 regulates zygotic genome activation in the mouse

Article Abstract:

Zygotic genome activation (ZGA), which is a nuclear reprogramming event that transforms the genome from transcriptional quiescence at fertilization to robust transcriptional activity is described. A maternal- effect mutation of Brg1, which encodes a catalytic subunit of SW1/SNF-related complexes, utilizing Cre-loxP gene targeting is generated.

Gene mutations, Gene mutation, Genetic regulation, Genetic research