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Riesle, A. J.

Publications and source records attributed to Riesle, A. J..

2 recordsLinked to original sources

The transcription of a single olfactory receptor per neuron is enforced by epigenetic silencing of their enhancers

The ability to discriminate thousands of odors in our environment requires each olfactory neuron to express a single olfactory receptor from hundreds of available genes. The biochemical mechanism enforcing this monogenic expression remains unknown. We show that deletion of the chromatin protein TRIM66 causes individual olfactory neurons to express multiple receptors at a high level, demonstrating that monogenic expression relies on an epigenetic silencing mechanism. Moreover, TRIM66 is specifically recruited to olfactory receptor gene super-enhancers during neuronal progenitor maturation, thereby silencing nearby olfactory receptor genes. Loss of monogenic expression disrupted axonal projections to the olfactory bulb, resulting in an aberrant topographic map and impaired social odor discrimination and reproductive behaviors. These findings uncover the chromatin-based silencing of super-enhancers as the mechanism underlying the organization of the mammalian olfactory system.

molecular biology↗

Activator-blocker model of transcriptional regulation by pioneer-like factors

Zygotic genome activation (ZGA) in the development of flies, fish, frogs and mammals depends on pioneer-like transcription factors (TFs). Those TFs create open chromatin regions, promote histone acetylation on enhancers, and activate transcription. Here, we use the panel of single, double and triple mutants for zebrafish genome activators Pou5f3, Sox19b and Nanog, multi-omics and mathematical modeling to investigate the combinatorial mechanisms of genome activation. We show that Pou5f3 and Nanog act differently on synergistic and antagonistic enhancer types. Pou5f3 and Nanog both bind as pioneer-like TFs on synergistic enhancers, promote histone acetylation and activate transcription. Antagonistic enhancers are activated by binding of one of these factors. The other TF binds as non-pioneer-like TF, competes with the activator and blocks all its effects, partially or completely. This activator-blocker mechanism mutually restricts widespread transcriptional activation by Pou5f3 and Nanog and prevents premature expression of late developmental regulators in the early embryo.

developmental biology↗