Conditional rod photoreceptor ablation reveals Sall1 as a microglial marker and regulator of microglial morphology in the retina

• DOI: 10.1002/glia.23038
• Publication Date: 2016-07-26T14:43:06Z
• Authors: Hideto Koso; Asano Tsuhako; Chen‐Yi Lai; Yukihiro Baba; Makoto Otsu; Kazuko Ueno; Masao Nagasaki; Yutaka Suzuki; Sumiko Watanabe
• Keywords: Monocyte; Phagocyte; Mononuclear phagocyte system

Neurodegeneration has been shown to induce microglial activation and the infiltration of monocyte‐derived macrophages into CNS, resulting in coexistence these two populations within same lesion, though their distinct features remain elusive. To investigate impact rod photoreceptor degeneration on activation, we generated a toxin‐mediated genetic model degeneration. Rod injury induced proliferation migration toward photoreceptors. Bone marrow transplantation revealed invasion retina, with microglia infiltrating showing distribution patterns retina. By comparing gene expression profiles activated macrophages, identified microglia‐specific genes, including Ak1 , Ctsf Sall1 Phlda3 Spns2 . An analysis Sall1gfp knock‐in mice showed GFP developing mature healthy retinas. DTA expansion + microglia, whereas Ly6C were mostly ‐ supporting idea that is exclusively expressed retinal phagocyte pool. We evaluated contribution pool rd1 mutant retinas found constituted majority phagocytes. A deficiency did not affect colonization retina cortex, but it change morphology from ramified more amoeboid appearance. The morphological defects observed ‐deficient rescued by presence wild‐type non‐microglial cells, suggesting functions cell‐autonomously microglia. Taken together, our data indicate regulates during development. GLIA 2016;64:2005–2024