C. elegans sirtuin SIR-2.4 and its mammalian homolog SIRT6 in stress response.

Stress is a significant life event. The immediate response to stress is critical for survival. In organisms ranging from the unicellular Saccharomyces cerevisiae to protozoa (Trypanosoma brucei) and metazoan (such as Caenorhabditis elegans, Homo sapiens) stress response leads to the formation of cytoplasmic RNA-protein complexes referred to as stress granules (SGs).

Histone H1 and heterochromatin protein 1 (HP1) regulate specific gene expression and not global transcription.

The highly conserved Hox transcription factors define positional identity along the anterior-posterior body axis during development. Inappropriate expression of Hox genes causes homeotic transformation, which leads to abnormal development of a specific region or segment. C.

The sirtuin SIRT6 regulates stress granule formation in C. elegans and mammals.

SIRT6 is a NAD(+)-dependent deacetylase that modulates chromatin structure and safeguards genomic stability. Until now, SIRT6 has been assigned to the nucleus and only nuclear targets of SIRT6 are known. Here, we demonstrate that in response to stress, C.

Mitochondrial SIRT4-type proteins in Caenorhabditis elegans and mammals interact with pyruvate carboxylase and other acetylated biotin-dependent carboxylases.

The biological and enzymatic function of SIRT4 is largely uncharacterized. We show that the Caenorhabditis elegans SIR-2.2 and SIR-2.

Transcriptional repression of Hox genes by C. elegans HP1/HPL and H1/HIS-24.

Elucidation of the biological role of linker histone (H1) and heterochromatin protein 1 (HP1) in mammals has been difficult owing to the existence of a least 11 distinct H1 and three HP1 subtypes in mice. Caenorhabditis elegans possesses two HP1 homologues (HPL-1 and HPL-2) and eight H1 variants. Remarkably, one of eight H1 variants, HIS-24, is important for C.

Novel roles of Caenorhabditis elegans heterochromatin protein HP1 and linker histone in the regulation of innate immune gene expression.

Linker histone (H1) and heterochromatin protein 1 (HP1) are essential components of heterochromatin which contribute to the transcriptional repression of genes. It has been shown that the methylation mark of vertebrate histone H1 is specifically recognized by the chromodomain of HP1. However, the exact biological role of linker histone binding to HP1 has not been determined.

Epigenetics in C. elegans: facts and challenges.

Epigenetics is defined as the study of heritable changes in gene expression that are not accompanied by changes in the DNA sequence. Epigenetic mechanisms include histone post-translational modifications, histone variant incorporation, non-coding RNAs, and nucleosome remodeling and exchange. In addition, the functional compartmentalization of the nucleus also contributes to epigenetic regulation of gene expression.

Interplay between histone deacetylase SIR-2, linker histone H1 and histone methyltransferases in heterochromatin formation.

Maintenance of intact heterochromatin structure through epigenetic mechanisms is essential for cell survival. Defects in heterochromatin formation caused by loss of chromatin-modifying enzymes lead to genomic instability and cellular senescence. The NAD(+)-dependent histone deacetylase SIR-2 and the H1 linker histone are intriguing chromatin elements that are connected to chromatin regulation and cell viability in the single cellular eukaryotic organism yeast.

Caenorhabditis elegans has a phosphoproteome atypical for metazoans that is enriched in developmental and sex determination proteins.

In eukaryotic species, signal transduction is often mediated by posttranslational modifications that can serve as regulatory switches. Although nematodes have usually been studied by genetic rather than biochemical methods, PTMs such as phosphorylation are thought to control all aspects of biological functions including sex determination and development. Here, we apply high accuracy mass spectrometry and comprehensive bioinformatic analysis to determine and characterize the in vivo Caenorhabditis elegans phosphoproteome for the first time.

HIS-24 linker histone and SIR-2.1 deacetylase induce H3K27me3 in the Caenorhabditis elegans germ line.

HIS-24 linker histone and SIR-2.1 deacetylase are involved in chromatin silencing in Caenorhabditis elegans. Depletion of SIR-2.