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Optimized Analysis of Proteins from Xenopus Oocytes and Embryos by Immunoblotting
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Split top: a maternal cathepsin B that regulates dorsoventral patterning and morphogenesis.

Yvette G Langdon1, Ricardo Fuentes2, Hong Zhang2

  • 1University of Pennsylvania Perelman School of Medicine, Department of Cell and Developmental Biology, 421 Curie Blvd., Philadelphia, PA 19104, USA Millsaps College, Department of Biology, Jackson, MS 39210, USA.

Development (Cambridge, England)
|February 20, 2016
PubMed
Summary

A maternal-effect zebrafish mutant, split top, reveals cathepsin Ba (ctsba) is crucial for embryonic dorsoventral patterning and morphogenesis. Loss of ctsba leads to dorsalized embryos and developmental defects, highlighting its novel role in early development.

Keywords:
BMPCathepsin BDorsoventralMaternal effectMorphogenesisZebrafish

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Area of Science:

  • Developmental biology
  • Genetics
  • Cell biology

Background:

  • Vertebrate embryonic axis formation relies on Wnt and bone morphogenetic protein (BMP) signaling.
  • Maternal factors regulate early Wnt signaling and influence zygotic BMP expression.
  • Maternal control of dorsoventral patterning and gastrulation morphogenesis is poorly understood.

Purpose of the Study:

  • To investigate maternal regulators of embryonic dorsoventral patterning and morphogenesis in zebrafish.
  • To identify genes essential for early embryonic development and tissue specification.
  • To elucidate the role of maternal factors in regulating BMP signaling and cell movements.

Main Methods:

  • Identification and characterization of the maternal-effect zebrafish mutant 'split top'.
  • Analysis of embryonic axis patterning and rescue experiments with BMP misexpression.
  • Chromosomal mapping and RNA sequencing to identify the causative gene.
  • Investigation of cytoskeletal organization and cell layer integrity.

Main Results:

  • Split top mutants exhibit a dorsalized embryonic axis, indicating disruption upstream of BMP signaling.
  • BMP misexpression or derepression can rescue the dorsalization phenotype.
  • Mutants display BMP-dependent and independent morphogenesis defects, including impaired dorsal convergence and delayed epiboly.
  • Cathepsin Ba (ctsba) was identified as the gene deficient in split top mutants.
  • Ctsba deficiency affects yolk cell cytoskeleton and outer enveloping cell layer, impacting epiboly.

Conclusions:

  • Cathepsin Ba (ctsba) plays a novel and essential role in zebrafish embryonic morphogenesis.
  • Ctsba is a critical maternal regulator of dorsoventral patterning and gastrulation.
  • This study expands understanding of maternal control over early vertebrate development and BMP signaling pathways.