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ZFIN ID: ZDB-PUB-180904-3
prpf4 is essential for cell survival and posterior lateral line primordium migration in zebrafish
Wang, Y., Han, Y., Xu, P., Ding, S., Li, G., Jin, H., Meng, Y., Meng, A., Jia, S.
Date: 2018
Source: Journal of genetics and genomics = Yi chuan xue bao   45(8): 443-453 (Journal)
Registered Authors: Jia, Shunji, Meng, Anming, Xu, Pengfei
Keywords: Apoptosis, Splicing, Zebrafish, pLLP, prpf4
MeSH Terms:
  • Animals
  • Apoptosis
  • Brain/cytology
  • Brain/metabolism
  • Cell Movement
  • Cell Survival
  • Gene Expression Regulation, Developmental
  • Introns
  • Lateral Line System/cytology
  • Lateral Line System/embryology
  • Lateral Line System/metabolism*
  • RNA Splicing
  • Signal Transduction
  • Spliceosomes/genetics
  • Spliceosomes/metabolism
  • Tumor Suppressor Protein p53/genetics
  • Tumor Suppressor Protein p53/metabolism
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 30174136 Full text @ J. Genet. Genomics
Prpf4 (pre-mRNA processing factor 4), a key component of spliceosome, plays critical roles in pre-mRNA splicing and its mutations result in retinitis pigmentosa due to photoreceptor defects. In this study, we characterized a zebrafish prpf4t243 mutant harboring a Tol2 transposon-based gene trap cassette in the third intron of the prpf4 gene. Cells in the brain and spinal cord gradually undergo p53-dependent apoptosis after 28 hpf in prpf4t243 mutants, suggesting that a widespread function of prpf4 in neural cell survival. In addition, prpf4 is essential for survival of posterior lateral line primordial (pLLP) cells. prpf4 deficiency perturbs Fgf, Wnt/β-catenin and chemokine signaling pathways and impairs pLLP migration. RNA-Seq analysis suggests that prpf4 deficiency may impair spliceosome assembly, leading to compensatory upregulation of core spliceosomal genes and alteration of pre-mRNA splicing. Taken together, our studies uncover an essential role of prpf4 in pre-mRNA splicing, cell survival and pLLP migration.