The cortical actin cytoskeleton of unactivated zebrafish eggs: Spatial organization and distribution of filamentous actin, nonfilamentous actin, and myosin-II

Becker, Karen A.; Hart, Nathan H.

doi:10.1002/(sici)1098-2795(199604)43:4<536::aid-mrd17>3.0.co;2-x

Cited by 30 publications

(13 citation statements)

References 56 publications

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“…Zebrafish eggs contain a cortical, sub-PM F-actin network that acts as a barrier to CGE prior to egg activation (Becker and Hart, 1996;Becker and Hart, 1999). Using rhodamine-phalloidin (RhPh) to label F-actin, we found that brom bones eggs displayed a relatively normal distribution of cortical F-actin prior to egg activation ( Fig.…”

Section: Brom Bones Mutants Exhibit Defective Cgementioning

confidence: 99%

“…These steps include the movement of granules to the plasma membrane (PM), fusion of the CG membranes with the PM, release of the granule contents, and conclude with membrane retrieval through compensatory endocytosis (Becker and Hart, 1999;Donovan and Hart, 1986). Dynamic changes in the actin cytoskeleton are crucial to allow the CGs to fuse with the PM, and subsequently retrieve the vacant CG membrane following exocytosis (Becker and Hart, 1996;Becker and Hart, 1999;Sokac et al, 2003). Since the CGE-driven processes of chorion elevation and hardening are impaired in brom bones mutant eggs, we investigated whether CGE was defective by examining actin cytoskeletal dynamics.…”

Section: Brom Bones Mutants Exhibit Defective Cgementioning

confidence: 99%

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hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish

et al. 2009

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2+-release messenger IP 3 , suggesting that brom bones is a regulator of IP 3 -mediated Ca 2+ release at fertilization. Interestingly, brom bones mutant embryos also display defects in dorsoventral axis formation accompanied by a disorganized cortical microtubule network, which is known to be crucial for dorsal axis formation. We provide evidence that the impaired microtubule organization is associated with non-exocytosed cortical granules from the earlier egg activation defect. Positional cloning of the brom bones gene reveals that a premature stop codon in the gene encoding hnRNP I (referred to here as hnrnp I) underlies the abnormalities. Our studies therefore reveal an important new role of hnrnp I in regulating the fundamental process of IP 3 -mediated Ca 2+ release at egg activation.

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Section: Brom Bones Mutants Exhibit Defective Cgementioning

confidence: 99%

Section: Brom Bones Mutants Exhibit Defective Cgementioning

confidence: 99%

hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish

et al. 2009

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“…In the zebrafish, egg activation is associated with a variety of processes such as changes in egg shape, ooplasmic segregation to the blastodisc, and cortical granule releasedependent chorion expansion (reviewed in Yamagani et al, 1992;Hart and Fluck, 1995; see also Becker and Hart, 1996;Becker and Hart 1999;Leung et al, 2000;Fern andez et al, 2006). Several zebrafish maternal-effect mutations (jump start, p11cv) have been identified that affect all of these processes, suggesting a function for the corresponding genes in upstream events in egg activation .…”

Section: Fertilizationmentioning

confidence: 99%

Vertebrate maternal‐effect genes: Insights into fertilization, early cleavage divisions, and germ cell determinant localization from studies in the zebrafish

Lindeman

Pelegri

2009

Molecular Reproduction Devel

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In the earliest stages of animal development prior to the commencement of zygotic transcription, all critical cellular processes are carried out by maternally‐provided molecular products accumulated in the egg during oogenesis. Disruption of these maternal products can lead to defective embryogenesis. In this review, we focus on maternal genes with roles in the fundamental processes of fertilization, cell division, centrosome regulation, and germ cell development with emphasis on findings from the zebrafish, as this is a unique and valuable model system for vertebrate reproduction. Mol. Reprod. Dev. 77: 299–313, 2010. © 2009 Wiley‐Liss, Inc.

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“…The zebrafish egg cortex is composed of a meshwork of actin filaments (Hart and Collins, 1991;Becker and Hart, 1996). During oogenesis, membrane-bound cortical granules (CGs) accumulate throughout this egg cortex (Hart et al, 1987;Mei et al, 2009), and activation of the egg through water exposure triggers rapid granule exocytosis (Hart and Collins, 1991;Becker and Hart, 1999).…”

Section: Introductionmentioning

confidence: 99%

aura/mid1ip1Lregulates the cytoskeleton at the zebrafish egg-to-embryo transition

2016

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Embryos from females homozygous for a recessive maternal-effect mutation in the gene aura exhibit defects including reduced cortical integrity, defective cortical granule (CG) release upon egg activation, failure to complete cytokinesis, and abnormal cell wound healing. Subcellular analysis shows that the cytokinesis defects observed in aura mutants are associated with aberrant cytoskeletal reorganization during furrow maturation, including abnormal F-actin enrichment and microtubule reorganization. Cortical F-actin prior to furrow formation fails to exhibit a normal transition into F-actin-rich arcs, and drug inhibition is consistent with aura function promoting F-actin polymerization and/or stabilization. In mutants, components of exocytic and endocytic vesicles, such as Vamp2, Clathrin and Dynamin, are sequestered in unreleased CGs, indicating a need for CG recycling in the normal redistribution of these factors. However, the exocytic targeting factor Rab11 is recruited to the furrow plane normally at the tip of bundling microtubules, suggesting an alternate anchoring mechanism independent of membrane recycling. A positional cloning approach indicates that the mutation in aura is associated with a truncation of Mid1 Interacting Protein 1L (Mid1ip1L), previously identified as an interactor of the X-linked Opitz G/BBB syndrome gene Mid1. A Cas9/CRISPR-induced mutant allele in mid1ip1L fails to complement the originally isolated aura maternal-effect mutation, confirming gene assignment. Mid1ip1L protein localizes to cortical F-actin aggregates, consistent with a direct role in cytoskeletal regulation. Our studies indicate that maternally provided aura/mid1ip1L acts during the reorganization of the cytoskeleton at the egg-to-embryo transition and highlight the importance of cytoskeletal dynamics and membrane recycling during this developmental period.

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The cortical actin cytoskeleton of unactivated zebrafish eggs: Spatial organization and distribution of filamentous actin, nonfilamentous actin, and myosin-II

Cited by 30 publications

References 56 publications

hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish

hnRNP I is required to generate the Ca2+ signal that causes egg activation in zebrafish

Vertebrate maternal‐effect genes: Insights into fertilization, early cleavage divisions, and germ cell determinant localization from studies in the zebrafish

aura/mid1ip1Lregulates the cytoskeleton at the zebrafish egg-to-embryo transition

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