Abstract
The nuclei of most vertebrate cells contain members of the high mobility group N (HMGN) protein family, which bind specifically to nucleosome core particles and affect chromatin structure and function, including transcription. Here, we study the biological role of this protein family by systematic analysis of phenotypes and tissue transcription profiles in mice lacking functional HMGN variants. Phenotypic analysis of Hmgn1(tm1/tm1), Hmgn3(tm1/tm1), and Hmgn5(tm1/tm1) mice and their wild type littermates with a battery of standardized tests uncovered variant-specific abnormalities. Gene expression analysis of four different tissues in each of the Hmgn(tm1/tm1) lines reveals very little overlap between genes affected by specific variants in different tissues. Pathway analysis reveals that loss of an HMGN variant subtly affects expression of numerous genes in specific biological processes. We conclude that within the biological framework of an entire organism, HMGNs modulate the fidelity of the cellular transcriptional profile in a tissue- and HMGN variant-specific manner.
Highlights
The ubiquitously expressed high mobility group N (HMGN) protein variants affect chromatin structure and transcription
HMGN proteins impact the cellular phenotype by modulating the transcription levels of numerous genes
Phenotypic analysis of Hmgn1tm1/tm1, Hmgn3tm1/tm1, and Hmgn5tm1/tm1 mice and their wild type littermates with a battery of standardized tests uncovered variant-specific abnormalities
Summary
We aimed to elucidate the biological significance of the interaction of each HMGN with chromatin; in all the Hmgntm1/tm mice, we deleted only the nucleosome binding domain of the respective HMGN variant, thereby abolishing its ability to bind to chromatin. This study aims to provide insights into this question by systematic analysis of phenotypes in mice lacking functional HMGN variants and through the biological context of whole tissue transcription profile analysis
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