CHD Chromatin Remodeling Protein Diversification Yields Novel Clades and Domains Absent in Classic Model Organisms

Abstract

Chromatin remodelers play a fundamental role in the assembly of chromatin, regulation of transcription, and DNA repair. Biochemical and functional characterization of the CHD family of chromatin remodelers from a variety of model organisms have shown that these remodelers participate in a wide range of activities. However, because the evolutionary history of CHD homologs is unclear, it is difficult to predict which of these activities are broadly conserved and which have evolved more recently in individual eukaryotic lineages. Here, we performed a comprehensive phylogenetic analysis of 8,042 CHD homologs from 1,894 species to create a model for the evolution of this family across eukaryotes with a particular focus on the timing of duplications that gave rise to the diverse copies observed in plants, animals, and fungi. Our analysis confirms that the three major subfamilies of CHD remodelers originated in the eukaryotic last common ancestor, and subsequent losses occurred independently in different lineages. Improved taxon sampling identified several subfamilies of CHD remodelers in plants that were absent or highly divergent in the model plant Arabidopsis thaliana. Whereas the timing of CHD subfamily expansions in vertebrates correspond to whole genome duplication events, the mechanisms underlying CHD diversification in land plants appears more complicated. Analysis of protein domains reveals that CHD remodeler diversification has been accompanied by distinct transitions in domain architecture, contributing to the functional differences observed between these remodelers. This study demonstrates the importance of proper taxon sampling when studying ancient evolutionary events to prevent misinterpretation of subsequent lineage-specific changes and provides an evolutionary framework for functional and comparative analysis of this critical chromatin remodeler family across eukaryotes.

PICKLE RELATED 2 is a Neofunctionalized Gene Duplicate Under Positive Selection With Antagonistic Effects to the Ancestral PICKLE Gene on the Seed Transcriptome

“…The three clades represented by PKL , PKR1 , and PKR3 are conserved between animals and plants, whereas PKR2 is the only plant-specific gene of the family and has been until now classified within the PKL clade for its close resemblance with PKL despite the lack of a PHD domain ( Ho et al 2013 ). We demonstrate here that PKR2 originated from a duplication of PKL during the early divergence of Brassicaceae, which is in agreement with Trujillo et al (2022) , and that PKR2 diverged from PKL . Our finding that PKR2 is under positive selection (while PKL is not) and that PKL seems to be relatively well-conserved across Embryophytes supports the possibility of a neofunctionalization of PKR2 .…”

Down syndrome child with multiple heart diseases: A case report

“…Endothelial progenitor cells maintain the stability of blood vessels and participate in the production of vascular endothelial cells[ 17 ]. Their dysfunction is mainly reflected in a reduction of cell number and physiological function, leading to damage in maintaining the stability of blood vessels and resulting in severe or irreversible damage in the early stages of pulmonary vessel development[ 18 ]. Furthermore, several studies have indicated higher levels of various inflammatory mediators in DS children, including tumor necrosis factor-α, interleukin-6, and C-reactive protein, among others.…”

“…Children with DS and CHD often experience repeated lung infections, weight loss, and advanced heart failure in the early stages before undergoing surgical treatment to correct cardiovascular malformations. Delayed treatment can result in an increased risk of mortality[ 16 - 18 ]. To investigate the status of DS with CHD over the past decade, we conducted a search of Chinese and international databases to identify cases who underwent surgical treatment.…”

Chromatin gatekeeper and modifier CHD proteins in development, and in autism and other neurological disorders

“…It has since been established that the fundamental function that is common to protein chromodomains is to interact with histones via the binding with methylated lysine residues of the histones (Micucci et al ., 2015). A comprehensive phylogenetic analysis revealed that most eukaryotic lineages have three CHD protein subfamilies, however, the dynamic evolution of this family of proteins has involved lineage-specific gains and losses, domain variations and structural modifications, suggesting these remodelers have evolved to meet specific roles in chromatin (Trujillo et al ., 2022). The CHD proteins are characterized by the presence of tandem N-terminal chromodomains and an SNF2-like ATPase domain in the center, and they are understood to be ATP-dependent chromatin remodelers.…”