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Bertran, J.

Publications and source records attributed to Bertran, J..

2 recordsLinked to original sources

Dynamic association of IκBα to chromatin is regulated by acetylation and cleavage of histone H4

I{kappa}Bs exert a principal function as cytoplasmic inhibitors of the NF-kB transcription factors. Additional functions for I{kappa}B homologues have been described including association to chromatin and transcriptional regulatioin. Phosphorylated and SUMOylated I{kappa}B (pS-I{kappa}B) binds histones H2A and H4 in the stem and progenitor compartment of skin and intestine, but the mechanisms controlling its recruitment to chromatin are largely unstudied. We here show that serine 32-36 phosphorylation of I{kappa}B favors its binding with nucleosomes and demonstrated that p-I{kappa}B association to H4 is favored by acetylation at specific H4 lysine residues. N-terminal tail of H4 is lost during intestinal cell differentiation by proteolytic cleavage at residues 17-19 imposed ny trypsin or chymotrypsin, which interferes p-I{kappa}B binding. Paradoxically, inhibition of trypsin and chymotrypsin activity in HT29 cells increased p-I{kappa}B chromatin binding and impaired goblet cell differentiation, comparable to I{kappa}B deletion. Together our results indicate that dynamic binding of I{kappa}B to chromatin is a requirement for intestinal cell differentiation and provide a molecular base for the restricted nuclear distribution of p-I{kappa}B at specific stem cell compartments.

molecular biology↗

Ancestral function of Inhibitors-of-kappaB regulates Caenorhabditis elegans development

Mammalian I{kappa}B proteins (I{kappa}Bs) exert their main function as negative regulators of NF-{kappa}B, a central signaling pathway controlling immunity and inflammation. An alternative chromatin role for I{kappa}Bs has been shown to affect stemness and cell differentiation. However, the involvement of NF-{kappa}B in this function has not been excluded. NFKI-1 and IKB-1 are I{kappa}B homologs in Caenorhabditis elegans, which lacks NF-{kappa}B nuclear effectors. We found that nfki-1 and ikb-1 mutants display developmental defects that phenocopy mutations in Polycomb and UTX-1 histone demethylase, suggesting a role for C. elegans I{kappa}Bs in chromatin regulation. Further supporting this possibility (i) we detected NFKI-1 in the nucleus of cells; (ii) NFKI-1 and IKB-1 bind to histones and Polycomb proteins, (iii) and associate with chromatin in vivo, and (iv) mutations in nfki-1 and ikb-1 alter chromatin marks. Based on these results, we propose that ancestral I{kappa}B inhibitors modulate Polycomb activity at specific gene subsets with an impact on development.

developmental biology↗