Chromosome-level genome assembly of the glass catfish(Kryptopterus vitreolus)reveals molecular clues to its transparent phenotype

Glass catfish(Kryptopterus vitreolus)are notable in the aquarium trade for their highly transparent body pattern.This transparency is due to the loss of most reflective iridophores and light-absorbing melanophores in the main body,although certain black and silver pigments remain in the face and head.To date,however,the molecular mechanisms underlying this transparent phenotype remain largely unknown.To explore the genetic basis of this transparency,we constructed a chromosome-level haplotypic genome assembly for the glass catfish,encompassing 32 chromosomes and 23344 protein-coding genes,using PacBio and Hi-C sequencing technologies and standard assembly and annotation pipelines.Analysis revealed a premature stop codon in the putative albinism-related tyrp1b gene,encoding tyrosinase-related protein 1,rendering it a nonfunctional pseudogene.Notably,a synteny comparison with over 30 other fish species identified the loss of the endothelin-3(edn3b)gene in the glass catfish genome.To investigate the role of edn3b,we generated edn3b^(−/−)mutant zebrafish,which exhibited a remarkable reduction in black pigments in body surface stripes compared to wild-type zebrafish.These findings indicate that edn3b loss contributes to the transparent phenotype of the glass catfish.Our high-quality chromosome-scale genome assembly and identification of key genes provide important molecular insights into the transparent phenotype of glass catfish.These findings not only enhance our understanding of the molecular mechanisms underlying transparency in glass catfish,but also offer a valuable genetic resource for further research on pigmentation in various animal species.

Using induced pluripotent stem cells for modeling Parkinson’s disease

Parkinson’s disease(PD)is an age-related neurodegenerative disease caused by the progressive loss of dopaminergic(DA)neurons in the substantia nigra.As DA neurons degenerate,PD patients gradually lose their ability of movement.To date no effective therapies are available for the treatment of PD and its pathogenesis remains unknown.Experimental models that appropriately mimic the development of PD are certainly needed for gaining mechanistic insights into PD pathogenesis and identifying new therapeutic targets.Human induced pluripotent stem cells(iPSCs)could provide a promising model for fundamental research and drug screening.In this review,we summarize various iPSCs-based PD models either derived from PD patients through reprogramming technology or established by gene-editing technology,and the promising application of iPSC-based PD models for mechanistic studies and drug testing.