Recommended reads: Shinya interview, MYC-MAX & extra digits, microglia as a therapy, oocyte maintenance

The proto-oncogene MYC is one of those factors studied in thousands of papers.

MYC and its dimerize partner MAX are also seemingly involved in just about everything. They have crucial roles in many kinds of stem cells including adult and embryonic stem cells. One way or another MYC induction seems very helpful for cellular reprogramming too.

I first really dove into studying MYC and by extension MAX as a postdoc in Bob Eisenman’s lab at The Hutch. I loved being a postdoc and having the opportunity to do all kinds of cool research. My work then included studies of MYC, MYCN, and the corepressor SIN3. With this background, I often find myself drawn to papers related to MYC so a new one related in part to digit development got my attention.

N-myc, heterochromatin, MYC
Loss of N-myc in neural stem cells leads to more heterochromatin. I found similar results with Myc too.


A recurrent de novo MAX p.Arg60Gln variant causes a syndromic overgrowth disorder through differential expression of c-Myc target genes, The American Journal of Human Genetics. One phenotypic take-home from this paper is: “Affected individuals have a complex disorder consisting primarily of macrocephaly, polydactyly, and delayed ophthalmic development.”

This one caught my eye in part because MYCN, which also dimerizes with MAX, has ties to digit developmental as well as polydactyly and syndactyly. For example, this old paper with my postdoctoral colleague and friend Peter Hurlin first made this MYCN connection. Activities of N-Myc in the developing limb link control of skeletal size with digit separation, Development. The macrocephaly part is intriguing too as MYC family loss of function, particularly for MYCN, causes the opposite: microcephaly. We first reported the role of MYCN loss of function in microcephaly in our 2002 G&D paper. Shortly after that, it was found that MYCN mutations cause microcephaly in humans. It was kind of amazing to see the connection between our mouse knockout work and a clinical syndrome in people.

I want to take this moment to thank an amazing senior scientist in Bob’s lab, Pei Feng Cheng, who was a major contributor to many of the studies on MYC family proteins.

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