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Mielnicka, M.

Publications and source records attributed to Mielnicka, M..

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↗

Trim66 paternal deficiency causes intrauterine overgrowth

The tripartite motif-containing protein 66 (TRIM66, also known as TIF1-delta) is a PHD-Bromo containing protein primarily expressed in post-meiotic male germ cells known as spermatids. Biophysical assays showed that TRIM66 PHD-Bromo domain binds to H3 N-terminus only when lysine 4 is unmethylated. We addressed TRIM66s role in reproduction by loss-of-function genetics in the mouse. Males homozygous for Trim66-null mutations produced functional spermatozoa. Round spermatids lacking TRIM66 upregulated a network of genes involved in histone acetylation and H3K4 methylation. Profiling of H3K4me3 patterns in the sperm produced by Trim66-null mutant showed minor alterations below statistical significance. Unexpectedly, Trim66-null males, but not females, sired pups overweight at birth, hence revealing that Trim66 mutations cause a paternal effect phenotype.

developmental biology↗