Brook T Chernet

In the 2014 paper with Levin, mRNAs for an oncogene and for the hyperpolarizing channel Kv1.5 were injected into separate blastomeres of 16-cell embryos. Embryos with a remote hyperpolarized region often lacked visible tumor-like structures, even though the oncogene protein was strongly expressed. Kv1.5 cut Xrel3 and Gli1 structures by about 35% and 29%, so the effect was not tied to one oncogene¹. High chloride, which also hyperpolarizes cells, reduced KRASG12D structures by 37.5%. The same paper reported leukocyte recruitment to transformed cells.

A second 2014 paper, with Chris Fields and Levin, asked whether gap-junctional communication links tumors to the host. Embryos injected with KRASG12D were given Lucifer Yellow, which passes gap junctions, and rhodamine dextran, which does not. Cells with yellow but no dextran signal showed open communication². The authors also built a two-stage quantitative model relating membrane voltage, gap-junctional communication and tumor formation, and used it to make numerical predictions.

Light was given early to prevent tumor-like structures, or at stages 28 to 35 to treat them. Stimulating ChR2D156A cells gave 31% more normalized tumors than unstimulated siblings³⁴. Levin later cited these papers as showing that oncogenes can be blocked by optogenetic or constitutive hyperpolarization⁵. A 2021 review cited the work as evidence of long-range physiological effects⁶. Chernet also appears in a 2012 acknowledgment for microscopy help.