OFCD syndrome and extraembryonic defects are revealed by conditional mutation of the Polycomb-group repressive complex 1.1 (PRC1.1) gene BCOR.

BCOR is a critical regulator of human development. Heterozygous mutations of BCOR in females cause the X-linked developmental disorder Oculofaciocardiodental syndrome (OFCD), and hemizygous mutations of BCOR in males cause gestational lethality. BCOR associates with Polycomb group proteins to form one subfamily of the diverse Polycomb repressive complex 1 (PRC1) complexes, designated PRC1.

Natriuretic peptide system expression in murine and human submandibular salivary glands: a study of the spatial localisation of ANB, BNP, CNP and their receptors.

The natriuretic peptide (NP) system comprises of three ligands, the Atrial Natriuretic Peptide (ANP), Brain Natriuretic peptide (BNP) and C-type Natriuretic peptide (CNP), and three natriuretic peptide receptors, NPRA, NPRB and NPRC. Here we present a comprehensive study of the natriuretic peptide system in healthy murine and human submandibular salivary glands (SMGs). We show CNP is the dominant NP in mouse and human SMG and is expressed together with NP receptors in ducts, autonomic nerves and the microvasculature of the gland, suggesting CNP autocrine signalling may take place in some of these glandular structures.

Molecular regulation of ocular gland development.

The tear film is produced by two ocular glands, the lacrimal glands, which produce the aqueous component of this film, and the meibomian glands, which secrete the lipidic component that is key to reduce evaporation of the watery film at the surface of the eye. Embryonic development of these exocrine glands has been mostly studied in mice, which also develop Harderian glands, a third type of ocular gland whose role is still not well understood. This review provides an update on the signalling pathways, transcription factors andextracellular matrix components that have been shown to play a role in ocular gland development.

Impact of hypofunctional occlusion on upper and lower molars after cessation of root development in adult mice.

Background: Hypofunctional occlusion is known to lead to changes in the length of roots over time. The mechanisms that drive such changes, however, are poorly understood, with most studies concentrating on juvenile rats prior to the arrest of root development. In this article, we investigated the response of the upper and lower first molar roots to lack of occlusion concentrating on time-points after the development of the roots has ceased using the mouse as a model.