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Nuclear reprogramming is the process of switching gene expression of one cell type to that of another cell type, usually from a differentiated cell state to an undifferentiated cell state. Differentiation occurs during processes such as development and morphogenesis, tissue regeneration, and malignancy. Cells can also be artificially induced to reprogram their gene expression by techniques such as nuclear transfer, induced pluripotency, and cell fusion. Such techniques have many applications in...
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Delayed transition to new cell fates during cellular reprogramming.

Xianrui Cheng1, Deirdre C Lyons2, Joshua E S Socolar3

  • 1Program in Computational Biology and Bioinformatics, Duke University, Durham, NC 27708, USA; Duke Center for Systems Biology, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708, USA.

Developmental Biology
|May 1, 2014
PubMed
Summary

Sea urchin embryos show cell fate reprogramming during gastrulation, replacing missing cell types. This developmental plasticity requires early specification gene activation for successful reprogramming.

Keywords:
Cell fateCell fate specificationDifferentiationGene regulatory networkRegulative developmentReprogrammingSea urchin embryo

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Area of Science:

  • Developmental biology
  • Evolutionary developmental biology
  • Cell biology

Background:

  • Cell fate specification in embryos can be reversed through reprogramming.
  • Understanding reprogramming offers insights into evolutionary developmental regulatory logic.
  • Sea urchin embryos exhibit remarkable cell plasticity during development.

Purpose of the Study:

  • To investigate the timing and requirements of cell fate reprogramming in the sea urchin embryo.
  • To understand the regulatory mechanisms underlying cell replacement after surgical manipulation.
  • To identify key genes and developmental stages involved in reprogramming.

Main Methods:

  • Surgical dissection of sea urchin embryos at different developmental stages.
  • Analysis of cell fate changes and replacement of missing cell types.
  • Gene expression analysis, including the use of morpholinos to knockdown specific genes (hox11/13b, foxA).

Main Results:

  • Cells in sea urchin gastrulae can reprogram to replace missing cell types, such as non-skeletogenic mesoderm (NSM) replacing skeletogenic mesoderm.
  • Reprogramming capability emerges at the early gastrula stage, even if cells were removed earlier.
  • Animal caps reprogrammed to replace endomesoderm, but this required prior contact with vegetal halves and activation of endomesoderm specification genes (hox11/13b, foxA).

Conclusions:

  • The capacity for cell fate reprogramming emerges at early gastrulation in sea urchin embryos.
  • Reprogramming requires the activation of early specification components of the target cell fates.
  • This study reveals critical insights into the developmental plasticity and regulatory logic governing cell fate decisions.