Journal article

MOZ directs the distal-less homeobox gene expression program during craniofacial development

Hannah K Vanyai, Alexandra Garnham, Rose E May, Helen M McRae, Caitlin Collin, Stephen Wilcox, Gordon K Smyth, Tim Thomas, Anne K Voss



Oral clefts are common birth defects. Individuals with oral clefts who have identical genetic mutations regularly present with variable penetrance and severity. Epigenetic or chromatin-mediated mechanisms are commonly invoked to explain variable penetrance. However, specific examples of these are rare. Two functional copies of the MOZ (KAT6A, MYST3) gene, encoding a MYST family lysine acetyltransferase chromatin regulator, are essential for human craniofacial development, but the molecular role of MOZ in this context is unclear. Using genetic interaction and genomic studies, we have investigated the effects of loss of MOZ on the gene expression program during mouse development. Among the mor..

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Awarded by Australian Government's National Health and Medical Research Council

Funding Acknowledgements

This work was funded by the Australian Government's National Health and Medical Research Council (grants 1010851, 1008699 and 1051078; research fellowships 1003435 to T.T., 575512 to A.K.V. and 1081421 and 1058892 to G.K.S.), by the Independent Research Institutes Infrastructure Support (IRIIS) Scheme, by Australian Postgraduate Awards (to H.K.V. and H.M.M.), by an Ian Potter Foundation Equipment Infrastructure Grant, and by a State Government of Victoria OIS (Operational Infrastructure Support) Grant.