Abstract

The germinal center (GC) microenvironment is the main source of memory B cells and plasma B cells that produce high-affinity antibodies. In the CG compartments the B cell proliferate and go through assembling of IG genes. A specific signaling pathway associate differentiation of B cells with that DNA damage. DNA damage induces the phosphorylation, inactivation and translocation to the cytoplasm of the transcriptional co-activator CRTC2, which results in down-regulation of a set of genes associated with proliferation. Preliminary results of our laboratory suggest that HDAC1 is related with the downregulation of these specific genes. Our principal goal is to evaluate the role of HDAC1 in the transcriptional regulation of CRTC2 target genes in B cells induced by DNA breaks.