Search bioRxiv⌕ Search

Biology subjects

Kompocholi, S.

Publications and source records attributed to Kompocholi, S..

2 recordsLinked to original sources

HDAC3 prevents enhancer hyperactivation to enable developmental transitions

Dynamic gene regulation requires precise cooperation between transcription factors and chromatin modifiers at regulatory elements to achieve not only activation or repression, but also appropriate transcript dosage. However, the molecular mechanisms that ensure developmental genes are transcribed at specific levels remain largely unknown. Here, we discover that the epigenetic repressor histone deacetylase 3 (HDAC3), together with co-activators, binds a subset of the most active putative enhancer elements. Using a tunable mouse embryonic stem cell degron system, we uncover that HDAC3 directly prevents enhancer--and consequently gene--overactivation, effectively establishing a molecular "speed limit" for many naive pluripotency and housekeeping genes. Interestingly, we find that both the catalytic and non-catalytic functions of HDAC3 contribute to establishing this physiological transcript dose. Specifically during early development, HDAC3 rather than functioning as a canonical repressor, constrains the activity of highly transcribed genes of the implanting epiblast and ensures timely exit from naive pluripotency in vitro. Altogether, this indicates that a dynamic equilibrium between activators and repressors coexists at highly active enhancer elements in pluripotent stem cells, establishing appropriate transcriptional dosage and rendering them responsive to signaling cues, thereby enabling timely and coordinated developmental progression.

developmental biology↗

RNA Polymerase II subunits overexpressions induce genome instability and deregulate transcription

Independently of the pathways or circuits deregulated in cancer cells, these present altered transcription patterns, often also direct consequence of deregulation of transcription factors. In this sense, also the RNA Polymerase complexes responsible for transcription can be affected in cancers. We find that upregulations of RNA Polymerase II subunits, especially the largest ones, correlates with poor cancer patients outcome across a range of tumor types, presenting increased genome instability. Overexpressing the subunits RPB1, RPB3 and RPB4 in cells we find that these induce DNA damage. However, the mechanisms behind this increased genome instability are specific for each subunit, linked to the unique transcription alterations generated by the subunit overexpression. Importantly, we find significant overlap between the genes with more DNA damage in our cell line models and those more affected in cancers with subunit upregulation, indicating that upregulations could be responsible for some of the phenotypes present in these patients.

molecular biology↗