PUBLICATION

Calcium transients accompany ooplasmic segregation in zebrafish embryos

Authors
Leung, C.F., S.E. Webb, and A.L. Miller
ID
ZDB-PUB-971111-3
Date
1998
Source
Development, growth & differentiation   40: 313-326 (Journal)
Registered Authors
Leung, Christina F., Miller, Andrew L., Webb, Sarah E.
Keywords
aequorin; calcium; ooplasmic segregation; zebrafish
MeSH Terms
  • Aequorin/metabolism
  • Aequorin/pharmacology
  • Animals
  • Buffers
  • Calcium/metabolism*
  • Calcium/pharmacology
  • Cell Division/drug effects
  • Cell Division/physiology
  • Cell Polarity/drug effects
  • Cytochalasin B/pharmacology
  • Cytoplasmic Streaming/drug effects
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/physiology
  • Female
  • Luminescent Measurements
  • Male
  • Microinjections
  • Ovum/chemistry
  • Ovum/drug effects
  • Ovum/physiology
  • Time Factors
  • Zebrafish/embryology*
PubMed
9639359 Full text @ Dev. Growth Diff.
Abstract
Through the injection of f-aequorin (a calcium-specific luminescent reporter), and the use of an imaging photon detector, transient localized elevations of free cytosolic calcium in the forming blastodisc (BD) and animal hemisphere cortex were visualized that correlated with ooplasmic segregation. The introduction of an appropriate concentration of the weak (KD = 1.5 micromol/L) calcium buffer 5,5'-dibromo-BAPTA results in the dissipation of these calcium domains, and inhibits cytoplasmic streaming and the subsequent formation of a BD at the animal pole. These inhibitory actions are dependent on the final cytosolic concentration of buffer within the egg: > or = 1.3 mmol/L blocks ooplasmic streaming; < 1.3 mmol/L eggs segregate normally. Injection of 5,5'-dimethyl-BAPTA (KD = 0.15 micromol/L) to a final concentration of 1.5 mmol/L as a control has no effect on ooplasmic streaming. These results suggest that localized domains of elevated free cytosolic calcium are essential for ooplasmic segregation in zebrafish. Furthermore, a hypothetical model is presented linking these calcium transients to the contraction of a cortically located actin microfilament network as a possible mechanism providing the driving force for segregation.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
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Orthology
Engineered Foreign Genes
Mapping