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Updated: Feb 5, 2026

Activity of Posterior Lateral Line Afferent Neurons during Swimming in Zebrafish
Published on: February 10, 2021
prpf4 is essential for cell survival and posterior lateral line primordium migration in zebrafish
Yixia Wang1, Yanchao Han1, Pengfei Xu1
1State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Insights
Pre-mRNA processing factor 4 (Prpf4) is vital for neural cell survival and migration in zebrafish. Its deficiency disrupts spliceosome function, leading to apoptosis and developmental defects.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- Pre-mRNA processing factor 4 (Prpf4) is a crucial spliceosome component.
- Mutations in Prpf4 are linked to retinitis pigmentosa.
- Zebrafish prpf4t243 mutant harbors a Tol2 transposon gene trap.
Purpose of the Study:
- To characterize the function of Prpf4 in zebrafish development.
- To investigate the role of Prpf4 in neural cell survival and migration.
- To understand the molecular mechanisms underlying Prpf4 deficiency.
Main Methods:
- Zebrafish prpf4t243 mutant characterization.
- Analysis of apoptosis in neural cells.
- Assessment of posterior lateral line primordial (pLLP) cell survival and migration.
- RNA-sequencing (RNA-Seq) analysis.
Main Results:
- prpf4t243 mutants exhibit p53-dependent apoptosis in brain and spinal cord cells.
- Prpf4 is essential for pLLP cell survival and migration.
- Prpf4 deficiency perturbs Fgf, Wnt/β-catenin, and chemokine signaling pathways.
- RNA-Seq reveals impaired spliceosome assembly and altered pre-mRNA splicing.
Conclusions:
- Prpf4 plays an essential role in pre-mRNA splicing and neural cell survival.
- Prpf4 is critical for posterior lateral line primordial cell migration.
- Prpf4 deficiency impacts multiple signaling pathways and spliceosome function.
Abstract:
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.
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