However, we cannot rule out the possibility that RP-associated splicing factors may possess unknown functions required only for processing some retina-specific transcripts and thus, a decrease in their expression or in their function due to genetic LDN-193189 supply mutations may lead to RP. In summary, our study showed that high levels of RP-associated splicing factors and snRNAs in mouse retinal cells correlate with the developmental regulation of the visual function. The high level of expression of these genes in retina may partially EX 527 explain the selective vulnerability of retinal cells in the case of RP18, 11 and 13. Although a minor splicing functional defect can be tolerated by mice which have a shorter life span, it may render an accumulative effect on retinal degeneration in humans. Although sleep is an essential behavioral process conserved across phyla from fruit flies to humans, its functions remain elusive. There are many theories about the function of sleep, including roles in metabolic balance, excitotoxic repair, and memory consolidation. The process of memory is also widely conserved in the animal kingdom, and the relationship between sleep and memory formation continues to be controversial. Studies in both rodents and Aplysia show a clear time-ofday effect on memory formation. In flies, short-term memory has been shown to be regulated by processes involving both circadian rhythms and sleep. In addition, a temporal window for the effects of sleep deprivation on memory has been shown in both invertebrate and vertebrate species. Four hours of sleep deprivation immediately following courtship training abolishes memory retention in flies, while SD later during the sleeping period has no effect. In rodents, REM SD either just before, or immediately after behavioral training, has been shown to abolish contextual memory formation. It has also been suggested that REM sleep is necessary during later consolidation periods of memory in rodents. While these results imply a role for sleep in the consolidation of memory, they describe the consequences of reducing sleep on the formation of memory. An alternate method for understanding the influence of sleep on memory formation would be to test the effects of augmenting sleep using genetic approaches. While molecular targets involving circadian- and sleep-dependent memory formation are beginning to be identified, specific molecular targets responsible for augmenting sleep and memory concomitantly are not known.