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Deficient induction response in a Xenopus nucleocytoplasmic hybrid.
Patrick Narbonne1, David E Simpson, John B Gurdon
1The Wellcome Trust/Cancer Research UK Gurdon Institute, The Henry Wellcome Building of Cancer and Developmental Biology, University of Cambridge, Cambridge, United Kingdom.
Plos Biology
|December 2, 2011
Summary
Nucleocytoplasmic incompatibility between frog species causes hybrid embryo developmental arrest. Inefficient signaling and protein differences, not genome activation, underlie defects, but treatments can partially rescue development.
Area of Science:
- Developmental biology
- Genetics
- Cell biology
Background:
- Hybrid and cybrid embryos often arrest development due to nuclear-cytoplasmic incompatibilities.
- Previous hypotheses focused on embryonic genome activation (EGA) or nucleo-mitochondrial issues.
- The precise causes of cybrid developmental defects remain unclear.
Purpose of the Study:
- To investigate the causes of developmental arrest in *Xenopus* cybrid embryos.
- To determine if embryonic genome activation (EGA) or signaling pathways are responsible for developmental failure.
- To identify specific molecular factors contributing to nucleocytoplasmic incompatibility.
Main Methods:
- Creation of androgenetic cybrids from *Xenopus laevis* egg cytoplasm and *Xenopus tropicalis* sperm.
- Assessment of embryonic genome activation (EGA) and energy levels in cybrids.
- Analysis of induction signaling from vegetal to animal cells and key protein (Xbra) concentrations.
- Partial rescue experiments using enhanced induction signals or Xbra signaling.
Main Results:
- Androgenetic cybrids invariably failed gastrulation and did not reach the tadpole stage.
- Cybrids exhibited normal EGA and energy levels despite gastrulation defects.
- Nucleocytoplasmic incompatibility resulted from reduced vegetal induction signals, decreased animal cell sensitivity, and altered Xbra protein levels.
- Gastrulation defects involved inefficient induction and defective convergence-extension.
- Partial rescue of induction and development was achieved with increased induction signals or Xbra signaling.
Conclusions:
- Egg cytoplasm from one species can fail to support development directed by the nucleus of another species, even with normal EGA.
- Developmental defects in cybrids stem from inefficient intercellular signaling and interspecies differences in key protein concentrations.
- These nucleocytoplasmic incompatibilities can be partially corrected through targeted treatments.
