Genetic Dissection of TAM Receptor-Ligand Interaction in Retinal Pigment Epithelial Cell Phagocytosis

Tal Burstyn-Cohen, Erin D. Lew, Paqui G. Través, Patrick G. Burrola, Joseph C. Hash, Greg Lemke

פרסום מחקרי: פרסום בכתב עתמאמרביקורת עמיתים

תקציר

Although TAM receptor tyrosine kinases play key roles in immune regulation, cancer metastasis, and viral infection, the relative importance of the two TAM ligands-Gas6 and Protein S-has yet to be resolved in any setting in vivo. We have now performed a genetic dissection of ligand function in the retina, where the TAM receptor Mer is required for the circadian phagocytosis of photoreceptor outer segments by retinal pigment epithelial cells. This process is severely attenuated in Mer mutant mice, which leads to photoreceptor death. We find that retinal deletion of either Gas6 or Protein S alone yields retinae with a normal number of photoreceptors. However, concerted deletion of both ligands fully reproduces the photoreceptor death seen in Mer mutants. These results demonstrate that Protein S and Gas6 function as independent, bona fide Mer ligands, and are, to a first approximation, interchangeable with respect to Mer-driven phagocytosis in the retina.

שפה מקוריתאנגלית אמריקאית
עמודים (מ-עד)1123-1132
מספר עמודים10
כתב עתNeuron
כרך76
מספר גיליון6
מזהי עצם דיגיטלי (DOIs)
סטטוס פרסוםפורסם - 20 דצמ׳ 2012
פורסם באופן חיצוניכן

ASJC Scopus subject areas

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