| First Author | Yamanaka T | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 12 | Pages | e84036 |
| PubMed ID | 24391875 | Mgi Jnum | J:211115 |
| Mgi Id | MGI:5574123 | Doi | 10.1371/journal.pone.0084036 |
| Citation | Yamanaka T, et al. (2013) Loss of aPKClambda in differentiated neurons disrupts the polarity complex but does not induce obvious neuronal loss or disorientation in mouse brains. PLoS One 8(12):e84036 |
| abstractText | Cell polarity plays a critical role in neuronal differentiation during development of the central nervous system (CNS). Recent studies have established the significance of atypical protein kinase C (aPKC) and its interacting partners, which include PAR-3, PAR-6 and Lgl, in regulating cell polarization during neuronal differentiation. However, their roles in neuronal maintenance after CNS development remain unclear. Here we performed conditional deletion of aPKClambda, a major aPKC isoform in the brain, in differentiated neurons of mice by camk2a-cre or synapsinI-cre mediated gene targeting. We found significant reduction of aPKClambda and total aPKCs in the adult mouse brains. The aPKClambda deletion also reduced PAR-6beta, possibly by its destabilization, whereas expression of other related proteins such as PAR-3 and Lgl-1 was unaffected. Biochemical analyses suggested that a significant fraction of aPKClambda formed a protein complex with PAR-6beta and Lgl-1 in the brain lysates, which was disrupted by the aPKClambda deletion. Notably, the aPKClambda deletion mice did not show apparent cell loss/degeneration in the brain. In addition, neuronal orientation/distribution seemed to be unaffected. Thus, despite the polarity complex disruption, neuronal deletion of aPKClambda does not induce obvious cell loss or disorientation in mouse brains after cell differentiation. |
