A mutation in the Cdon gene potentiates congenital nevus development mediated by NRASQ61K

A. Chitsazan, B. Ferguson, Ramesh Ram, P. Mukhopadhyay, H.Y. Y. Handoko, B. Gabrielli, P.H. H. Soyer, Grant Morahan, G.J. J. Walker

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


Congenital nevi develop before birth and sometimes cover large areas of the body. They are presumed to arise from the acquisition of a gene mutation in an embryonic melanocyte that becomes trapped in the dermis during development. Mice bearing the Cdk4R24C::Tyr-NRASQ 61K transgenes develop congenital nevus-like lesions by post-natal day 10, from melanocytes escaping the confines of hair follicles. We interbred these mice with the collaborative cross (CC), a resource that enables identification of modifier genes for complex diseases (those where multiple genes are involved). We examined variation in nevus cell density in 66 CC strains and mapped a large-effect quantitative trait locus (QTL) controlling nevus cell density to murine chromosome 9. The best candidate for a gene that exacerbates congenital nevus development in the context of an NRAS mutation is Cdon, a positive regulator of sonic hedgehog (Shh) that is expressed mainly in keratinocytes. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Original languageEnglish
Pages (from-to)459-464
Number of pages6
Issue number4
Publication statusPublished - 1 Jul 2016


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