bioRxiv ScienceSearch

Biology subjects

Chung, W.-S.

Publications and source records attributed to Chung, W.-S..

2 recordsLinked to original sources

Seeing Nemo: molecular evolution of ultraviolet visual opsins and spectral tuning of photoreceptors in anemonefishes (Amphiprioninae)

Many animals can see ultraviolet (UV) light (shorter than 400 nm) undetectable to human vision. UV vision may have functional importance in many taxa including for foraging and communication in birds, reptiles, insects and teleost fishes. Shallow coral reefs transmit a broad spectrum of light and are rich in UV; driving the evolution of diverse spectral sensitivities in teleost reef fishes, including UV-sensitivity. However, the identities and sites of the specific visual genes that underly vision in reef fishes remain elusive and are useful in determining how molecular evolution has tuned vision to meet the ecological demands of life on the reef. We investigated the visual systems of eleven anemonefish (Amphiprioninae) species, specifically probing for the molecular pathways that facilitate UV-sensitivity. Searching the genomes of anemonefishes, we identified a total of seven functional visual genes from all five vertebrate opsin gene subfamilies. We found rare instances of UV-sensitive SWS1 opsin gene duplications, that produced two functional paralogs (SWS1 and SWS1{beta}) and a pseudogene. We also found separate RH2A opsin gene duplicates not yet reported in the family Pomacentridae. Finally, we report on both qualitative and quantitative aspects of opsin gene expression found in the adult retina of the false clown anemonefish (Amphiprion ocellaris), and their photoreceptor spectral sensitivities measured using microspectrophotometry.

molecular biology

CDC50A dependent phosphatidylserine exposure induces inhibitory post-synapse elimination by microglia

Glia contribute to synapse elimination through phagocytosis in the central nervous system. Despite important roles during development and neurological disorders, the "eat-me" signal that initiates glia-mediated phagocytosis of synapses remains largely elusive. Here, by generating inducible conditional knockout mice of Cdc50a, we induced stable exposure of phosphatidylserine in the neuronal outer membrane. Surprisingly, acute Cdc50a deletion in neurons causes specific loss of inhibitory post-synapses without affecting other synapses, thereby generating excessive excitability with appearance of seizure. Ablating microglia or deleting microglial Mertk rescues the loss of inhibitory post-synapses, indicating that microglial phagocytosis is responsible for inhibitory post-synapse elimination. Moreover, inhibitory post-synapses in normal juvenile brains also use phosphatidylserine for synapse pruning by microglia, suggesting that phosphatidylserine may serve as a general "eat-me" signal for inhibitory post-synapse elimination. One Sentence SummaryCdc50a dependent phosphatidylserine exposure functions as an "eat-me" signal for microglia-dependent inhibitory post-synapse elimination

neuroscience