Processivity and specificity of histone acetylation by the male-specific lethal complex.

Acetylation of lysine 16 of histone H4 (H4K16ac) stands out among the histone modifications, because it decompacts the chromatin fiber. The metazoan acetyltransferase MOF (KAT8) regulates transcription through H4K16 acetylation. Antibody-based studies had yielded inconclusive results about the selectivity of MOF to acetylate the H4 N-terminus.

Physical interaction between MSL2 and CLAMP assures direct cooperativity and prevents competition at composite binding sites.

MSL2, the DNA-binding subunit of the Drosophila dosage compensation complex, cooperates with the ubiquitous protein CLAMP to bind MSL recognition elements (MREs) on the X chromosome. We explore the nature of the cooperative binding to these GA-rich, composite sequence elements in reconstituted naïve embryonic chromatin. We found that the cooperativity requires physical interaction between both proteins.

Divergent evolution toward sex chromosome-specific gene regulation in .

The dosage compensation complex (DCC) of identifies its X-chromosomal binding sites with exquisite selectivity. The principles that assure this vital targeting are known from the model: DCC-intrinsic specificity of DNA binding, cooperativity with the CLAMP protein, and noncoding roX2 RNA transcribed from the X chromosome. We found that in , a species separated from by 40 million years of evolution, all principles are active but contribute differently to X specificity.

SWR1 and NuA4 complexes are defined by DOMINO isoforms.

Histone acetylation and deposition of H2A.Z variant are integral aspects of active transcription. In , the single DOMINO chromatin regulator complex is thought to combine both activities an unknown mechanism.

Micronuclei-based model system reveals functional consequences of chromothripsis in human cells.

Cancer cells often harbor chromosomes in abnormal numbers and with aberrant structure. The consequences of these chromosomal aberrations are difficult to study in cancer, and therefore several model systems have been developed in recent years. We show that human cells with extra chromosome engineered via microcell-mediated chromosome transfer often gain massive chromosomal rearrangements.