| First Author | Rao SB | Year | 2019 |
| Journal | Glia | Volume | 67 |
| Issue | 6 | Pages | 1138-1149 |
| PubMed ID | 30803043 | Mgi Jnum | J:274735 |
| Mgi Id | MGI:6287542 | Doi | 10.1002/glia.23600 |
| Citation | Rao SB, et al. (2019) Targeted deletion of beta1-syntrophin causes a loss of Kir 4.1 from Muller cell endfeet in mouse retina. Glia 67(6):1138-1149 |
| abstractText | Proper function of the retina depends heavily on a specialized form of retinal glia called Muller cells. These cells carry out important homeostatic functions that are contingent on their polarized nature. Specifically, the Muller cell endfeet that contact retinal microvessels and the corpus vitreum show a tenfold higher concentration of the inwardly rectifying potassium channel Kir 4.1 than other Muller cell plasma membrane domains. This highly selective enrichment of Kir 4.1 allows K+ to be siphoned through endfoot membranes in a special form of spatial buffering. Here, we show that Kir 4.1 is enriched in endfoot membranes through an interaction with beta1-syntrophin. Targeted disruption of this syntrophin caused a loss of Kir 4.1 from Muller cell endfeet without affecting the total level of Kir 4.1 expression in the retina. Targeted disruption of alpha1-syntrophin had no effect on Kir 4.1 localization. Our findings show that the Kir 4.1 aggregation that forms the basis for K+ siphoning depends on a specific syntrophin isoform that colocalizes with Kir 4.1 in Muller endfoot membranes. |
