Silent chromatin at the middle and ends: lessons from yeasts

Eukaryotic centromeres and telomeres are specialized chromosomal regions that share one common characteristic: their underlying DNA sequences are assembled into heritably repressed chromatin. Silent chromatin in budding and fission yeast is composed of fundamentally divergent proteins tat assemble very different chromatin structures. However, the ultimate behaviour of silent chromatin and the pathways that assemble it seem strikingly similar among Saccharomyces cerevisiae (S. cerevisiae), Schizosaccharomyces pombe (S. pombe) and other eukaryotes. Thus, studies in both yeasts have been instrumental in dissecting the mechanisms that establish and maintain silent chromatin in eukaryotes, contributing substantially to our understanding of epigenetic processes. In this review, we discuss current models for the generation of heterochromatic domains at centromeres and telomeres in the two yeast species

H3 Lysine 4 Is Acetylated at Active Gene Promoters and Is Regulated by H3 Lysine 4 Methylation

Methylation of histone H3 lysine 4 (H3K4me) is an evolutionarily conserved modification whose role in the regulation of gene expression has been extensively studied. In contrast, the function of H3K4 acetylation (H3K4ac) has received little attention because of a lack of tools to separate its function from that of H3K4me. Here we show that, in addition to being methylated, H3K4 is also acetylated in budding yeast. Genetic studies reveal that the histone acetyltransferases (HATs) Gcn5 and Rtt109 contribute to H3K4 acetylation in vivo. Whilst removal of H3K4ac from euchromatin mainly requires the histone deacetylase (HDAC) Hst1, Sir2 is needed for H3K4 deacetylation in heterochomatin. Using genome-wide chromatin immunoprecipitation (ChIP), we show that H3K4ac is enriched at promoters of actively transcribed genes and located just upstream of H3K4 tri-methylation (H3K4me3), a pattern that has been conserved in human cells. We find that the Set1-containing complex (COMPASS), which promotes H3K4me2 and -me3, also serves to limit the abundance of H3K4ac at gene promoters. In addition, we identify a group of genes that have high levels of H3K4ac in their promoters and are inadequately expressed in H3-K4R, but not in set1Δ mutant strains, suggesting that H3K4ac plays a positive role in transcription. Our results reveal a novel regulatory feature of promoter-proximal chromatin, involving mutually exclusive histone modifications of the same histone residue (H3K4ac and H3K4me)

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Not AvailableThe study describes prevalence, clinical symptoms and risk factors for brucellosis in personnel engaged in veterinary health care in Karnataka, India. A total of 1050 sera samples were collected from animal handlers, veterinarians, veterinary students, para-veterinarians and persons engaged in artificial insemination of animals. The sera samples were tested for brucellosis by Rose Bengal plate test (RBPT), serum agglutination test (SAT), IgG and IgM indirect ELISA and PCR. Age, sex, clinical symptoms and risk factors were recorded in structured questionnaire. Of the 1050 samples tested, 6.76, 6.38, 3.90, 2.67 and 2.0% were positive by IgG ELISA, RBPT, SAT, IgM ELISA and PCR, respectively and overall prevalence recorded was 7.04%. The prominent clinical symptoms observed were intermittent fever (71.62%) followed by joint pain and body aches. A high degree of suspicion, awareness and multimodal diagnostic approach is suggested for early diagnosis, treatment and disease follow up.Not Availabl

Stress-induced changes in sleep and associated neuronal activity in rat hippocampus and amygdala

Stress increases vulnerability to anxiety and depression. We have investigated the effect of acute immobilization stress in amygdalohippocampal circuits by measuring the Electroencephalogram (EEG) in male Wistar rats during Rapid Eye Movement (REM) sleep. Electrodes were implanted stereotaxically in the hippocampus (CA1 and CA3 subregions of the hippocampus) and the amygdala (lateral nucleus). Prior to the stress, two baseline recordings were taken. Twenty-four hours later rats were exposed once to Acute Immobilization Stress (AIS) session for 2 h. After the release and on subsequent days, electrophysiological changes that occurred due to stress during REM sleep were analyzed by comparing them with baseline measurements. Our results suggest that acute immobilization stress induced significant increase in REM sleep in the first 24 h after the exposure. In addition to changes in the sleep patterns, we have observed increased θ oscillations in CA1 area of the hippocampus with decreased coherence at θ range (4–8 Hz) between hippocampus and amygdala. These results suggest that single exposure to aversive experience such as immobilization stress can lead to dynamic changes in neuronal activities with altered sleep morphology. The results obtained in the present study are comparable to those seen in human patients suffering from panic, and anxiety due to Posttraumatic Stress Disorder (PTSD)