| First Author | Yang SB | Year | 2012 |
| Journal | J Physiol | Volume | 590 |
| Issue | 11 | Pages | 2645-58 |
| PubMed ID | 22411008 | Mgi Jnum | J:197275 |
| Mgi Id | MGI:5491996 | Doi | 10.1113/jphysiol.2012.228486 |
| Citation | Yang SB, et al. (2012) Kv1.1-dependent control of hippocampal neuron number as revealed by mosaic analysis with double markers. J Physiol 590(Pt 11):2645-58 |
| abstractText | Megencephaly, or mceph, is a spontaneous frame-shift mutation of the mouse Kv1.1 gene. This mceph mutation results in a truncated Kv1.1 channel alpha-subunit without the channel pore domain or the voltage sensor. Interestingly, mceph/mceph mouse brains are enlarged and - unlike wild-type mouse brains - they keep growing throughout adulthood, especially in the hippocampus and ventral cortex. We used mosaic analysis with double markers (MADM) to identify the underlying mechanism. In mceph-MADM6 mice with only a small fraction of neurons homozygous for the mceph mutation, those homozygous mceph/mceph neurons in the hippocampus are more abundant than wild-type neurons produced by sister neural progenitors. In contrast, neither mceph/mceph astrocytes, nor neurons in the adjacent dorsal cortex (including the entorhinal and parietal cortex) exhibited overgrowth in the adult brain. The sizes of mceph/mceph hippocampal neurons were comparable to mceph/+ or wild-type neurons. Our mosaic analysis reveals that loss of Kv1.1 function causes an overproduction of hippocampal neurons, leading to an enlarged brain phenotype. |
