Altering a histone H3K4 methylation pathway in glomerular podocytes promotes a chronic disease phenotype.

ABSTRACT: Methylation of specific lysine residues in core histone proteins is essential for embryonic development and can impart active and inactive epigenetic marks on chromatin domains. The ubiquitous nuclear protein PTIP is encoded by the Paxip1 gene and is an essential component of a histone H3 lysine 4 (H3K4) methyltransferase complex conserved in metazoans. In order to determine if PTIP and its associated complexes are necessary for maintaining stable gene expression patterns in a terminally differentiated, non-dividing cell, we conditionally deleted PTIP in glomerular podocytes in mice. Renal development and function were not impaired in young mice. However, older animals progressively exhibited proteinuria and podocyte ultra structural defects similar to chronic glomerular disease. Loss of P

SUBMITTER: Lefevre GM 

PROVIDER: S-EPMC2965754 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature