Background:The mechanisms that control the Prrxl1 expression are poorly understood. Results: Several regulatory elements present in Prrxl1 alternative promoters are functionally characterized, including a binding motif for Phox2b required for Prrxl1 expression in visceral sensory neurons. Conclusion: We define diverse regulatory modules, which control the spatiotemporal expression of Prrxl1 in nociceptive neurons. Significance: A new mechanism involved in the ganglion specific action of Prrxl1 is described.

Highlights d Histone 3 lysine 14 is essential and required for developmental patterning d H3K14ac decorates a set of tissue-specific genes that lack canonical histone marks d H3K14 is necessary for expression of genes marked uniquely by H3K14 acetylation d H3K14ac is recognized by the Brahma bromodomain

The histone deacetylase HDAC3 is associated with the NCoR/SMRT co-repressor complex and its canonical function is in transcriptional repression, but it can also activate transcription. Here we show that the repressor and activator functions of HDAC3 can be genetically separated in Drosophila. A lysine substitution in the N-terminus (K26A) disrupts its catalytic activity and activator function, whereas a combination of substitutions (HEBI) abrogating the interaction with SMRTER enhance repressor activity beyond wild-type in the early embryo. We conclude that the critical functions of HDAC3 in embryo development involve catalytic-dependent gene activation and non-enzymatic repression by several mechanisms, including tethering of loci to the nuclear periphery.

Highlights d Histone 3 lysine 14 is essential and required for developmental patterning d H3K14ac decorates a set of tissue-specific genes that lack canonical histone marks d H3K14 is necessary for expression of genes marked uniquely by H3K14 acetylation d H3K14ac is recognized by the Brahma bromodomain

No abstract

The histone deacetylase HDAC3 is associated with the NCoR/SMRT co-repressor complex and its canonical function is in transcriptional repression, but it can also activate transcription. Here we show that the repressor and activator functions of HDAC3 can be genetically separated in Drosophila. A lysine substitution in the N-terminus (K26A) disrupts its catalytic activity and activator function, whereas a combination of substitutions (HEBI) abrogating the interaction with SMRTER enhance repressor activity beyond wild-type in the early embryo. We conclude that the critical functions of HDAC3 in embryo development involve catalytic-dependent gene activation and non-enzymatic repression by several mechanisms, including tethering of loci to the nuclear periphery.

No abstract

mean fold change: 2.7) in comparison to a group of control individuals; the expression of the CDKL5 gene was similar to that of controls (mean fold change: 0.95). We are currently investigating the molecular mechanisms that lead to this de-regulation of the expression of the MECP2 gene in the absence of exonic structural changes. We propose this de-regulation of expression may underlie disease in other RTT-like patients who test negative for MECP2 mutations.