Issue Cover (February 2019)

Front cover: Transmembrane protein 30A (TMEM30A) acts as a β‐subunit for membrane phosphatidylserine (PS) flippases which are responsible for the asymmetric distribution of PS between the cytoplasmic leaflet and the exoplasmic leaflet of the membrane bilayer. Tmem30a is widely expressed in retina and is essential for photoreceptor survival. Tmem30a rod bipolar cell (RBC) knockout mice were established using CreloxP system to access the role of Tmem30a in mouse RBCs. Tmem30a deletion impaired the synaptic efficacy of mouse retinal rod bipolar cells, which led to the ectopic dendritic spouting. An activated inflammatory reaction induced by retinal glia also contributed to the degenerationof rod bipolar cells. This study implies an essential role of Tmem30a and PS asymmetry in RBC integrity and function. Image Content: Tmem30a RBC knockout mice were established using Cre‐loxP system. A tdTomato reporter was used to monitor the efficiency of Cre‐mediated deletion. The reporter contains a loxP‐flanked STOP cassette that prevents transcription of the downstreamCAG promoter‐driven red fluorescent protein variant tdTomato. In the presence of Cre recombinase, the STOP cassette is removed in Creexpressing tissue(s) and tdTomato is expressed. This image shows that tdTomato (red) was expressed specifically in PKCα‐positive rod bipolar cells (green). Nuclei were stained with 4′,6‐diamidino‐2‐phenylin (DAPI).Read the full article ‘ Tmem30a deficiency leads to retinal rod bipolar cell degeneration’ by Y. Yang, W. Liu, K. Sun, L. Jiang, X. Zhu ( J. Neurochem. 2019, vol. 148 (3), pp. 400–412) on doi: 10.1111/jnc.14643