ArticlePLoS genetics2014
Souffle/Spastizin controls secretory vesicle maturation during zebrafish oogenesis.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Maternal Huluwa regulates postfertilization microtubule array organization for asymmetrical transport of dorsal determinants in zebrafish.Nature communications · 2026Article
- Comparative proteomic analysis of the zebrafish (Danio rerio) perivitelline fluid; identifying putative cortical alveoli-associated proteins.Biology of reproduction · 2026Article
- Review
- Patient-specific mutation of contact site protein Tomm70 causes neurodegeneration.Disease models & mechanisms · 2025Article
- Phenogenetics of cortical granule dynamics during zebrafish oocyte-to-embryo transition.Frontiers in cell and developmental biology · 2025Review
- Axon demyelination and degeneration in a zebrafishOpen biology · 2024Article
- Maternal regulation of the vertebrate oocyte-to-embryo transition.PLoS genetics · 2024Article
- Diving deep: zebrafish models in motor neuron degeneration research.Frontiers in neuroscience · 2024Review
- Yolk granule fusion and microtubule aster formation regulate cortical granule translocation and exocytosis in zebrafish oocytes.PLoS biology · 2023Article
- Autophagic lysosome reformation in health and disease.Autophagy · 2023Review
- Knockin' on Egg's Door: Maternal Control of Egg Activation That Influences Cortical Granule Exocytosis in Animal Species.Frontiers in cell and developmental biology · 2021Review
- Janus-faced spatacsin (SPG11): involvement in neurodevelopment and multisystem neurodegeneration.Brain : a journal of neurology · 2020Review
- Article
- Fishing forward and reverse: Advances in zebrafish phenomics.Mechanisms of development · 2018Review
- Double maternal-effect: duplicated nucleoplasmin 2 genes, npm2a and npm2b, with essential but distinct functions are shared by fish and tetrapods.BMC evolutionary biology · 2018Article
- Inhibition of Lysosome Membrane Recycling Causes Accumulation of Gangliosides that Contribute to Neurodegeneration.Cell reports · 2018Article
- Functional Manipulation of Maternal Gene Products Using In Vitro Oocyte Maturation in Zebrafish.Journal of visualized experiments : JoVE · 2017Article
- aura (mid1ip1l) regulates the cytoskeleton at the zebrafish egg-to-embryo transition.Development (Cambridge, England) · 2016Article
- mTOR activates the VPS34-UVRAG complex to regulate autolysosomal tubulation and cell survival.The EMBO journal · 2015Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During oogenesis, the egg prepares for fertilization and early embryogenesis. As a consequence, vesicle transport is very active during vitellogenesis, and oocytes are an outstanding system to study regulators of membrane trafficking. Here, we combine zebrafish genetics and the oocyte model to identify the molecular lesion underlying the zebrafish souffle (suf) mutation. We demonstrate that suf encodes the homolog of the Hereditary Spastic Paraplegia (HSP) gene SPASTIZIN (SPG15). We show that in zebrafish oocytes suf mutants accumulate Rab11b-positive vesicles, but trafficking of recycling endosomes is not affected. Instead, we detect Suf/Spastizin on cortical granules, which undergo regulated secretion. We demonstrate genetically that Suf is essential for granule maturation into secretion competent dense-core vesicles describing a novel role for Suf in vesicle maturation. Interestingly, in suf mutants immature, secretory precursors accumulate, because they fail to pinch-off Clathrin-coated buds. Moreover, pharmacological inhibition of the abscission regulator Dynamin leads to an accumulation of immature secretory granules and mimics the suf phenotype. Our results identify a novel regulator of secretory vesicle formation in the zebrafish oocyte. In addition, we describe an uncharacterized cellular mechanism for Suf/Spastizin activity during secretion, which raises the possibility of novel therapeutic avenues for HSP research.
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