Loss of diurnal arrestin gene expression in rds mutant mouse retinas.
Despite the important advances in the molecular analysis of retinal degenerations, the causes of photoreceptor cell death in these conditions are unclear. To explore the metabolic impact of the rds mutation, we have continued our investigations on the expression of arrestin. Normal BALB/c mouse retinas have a diurnal variation in arrestin gene expression and protein biosynthesis, with low levels in dark-adapted and high levels in the light-adapted retinas. In contrast, arrestin is expressed in rds retinas at high levels throughout the diurnal cycle. A lack of a distinct diurnal cycle and continuously high expression of arrestin in rds retinas might be a reflection of metabolic derangements in these cells which are not an obvious consequence of the underlying molecular defect in the rds/peripherin gene.
Agarwal
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Department of Pathology, University of Texas Health Science Center at San Antonio 78284.
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Papermaster
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D000221:Adaptation, Ocular / Q000502:physiology; D000818:Animals; D000941:Antigens / Q000096:biosynthesis* / Q000235:genetics; D019393:Arrestin; D015152:Blotting, Northern; D002940:Circadian Rhythm; D005136:Eye Proteins / Q000096:biosynthesis* / Q000235:genetics; D015870:Gene Expression; D066298:In Vitro Techniques; D051379:Mice; D008807:Mice, Inbred BALB C; D008817:Mice, Mutant Strains; D012333:RNA, Messenger / Q000096:biosynthesis; D012160:Retina / Q000378:metabolism; D012162:Retinal Degeneration / Q000235:genetics* / Q000378:metabolism
D000941:Antigens; D019393:Arrestin; D005136:Eye Proteins; D012333:RNA, Messenger