Baker Scott T, Turgeon Shane M, Tulgren Erik D, Wigant Jeanne, Rahimi Omeed, Opperman Karla J, Grill Brock
Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458 Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455.
Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458.
Genetics. 2015 Jan;199(1):151-6. doi: 10.1534/genetics.114.170589. Epub 2014 Oct 22.
We show that loss-of-function mutations in kinases of the MLK-1 pathway (mlk-1, mek-1, and kgb-1/jnk) function cell-autonomously in neurons to suppress defects in synapse formation and axon termination caused by rpm-1 loss of function. Our genetic analysis also suggests that the phosphatase PPM-1, like RPM-1, is a potential inhibitor of kinases in the MLK-1 pathway.
我们发现,MLK-1通路的激酶(mlk-1、mek-1和kgb-1/jnk)功能缺失突变在神经元中自主发挥作用,以抑制因rpm-1功能缺失而导致的突触形成和轴突终末缺陷。我们的遗传学分析还表明,磷酸酶PPM-1与RPM-1一样,是MLK-1通路中激酶的潜在抑制剂。