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ADAR1-Dependent RNA Editing Promotes MET and iPSC Reprogramming by Alleviating ER Stress.

Diana Guallar1, Alejandro Fuentes-Iglesias2, Yara Souto2

  • 1Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), Universidade de Santiago de Compostela (USC)-Health Research Institute (IDIS), Santiago de Compostela 15782, Spain; Department of Biochemistry and Molecular Biology, USC, Santiago de Compostela 15782, Spain.

Cell Stem Cell
|May 13, 2020
PubMed
Summary
This summary is machine-generated.

Loss of ADAR1-mediated RNA editing disrupts stem cell reprogramming by hindering mesenchymal-to-epithelial transition. This impairs pluripotency acquisition due to aberrant immune responses and endoplasmic reticulum stress.

Keywords:
ADAR1ER stressMETRNA A-to-I editingUPRiPSCinnate immune responsepluripotencysomatic cell reprogrammingsubcellular localization

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Area of Science:

  • Molecular Biology
  • Stem Cell Biology
  • Epigenetics

Background:

  • Adenosine to inosine (A to I) RNA editing, catalyzed by ADAR1, significantly modifies the transcriptome.
  • The role of ADAR1-mediated RNA editing in somatic cell reprogramming remains largely uncharacterized.

Purpose of the Study:

  • To investigate the functional role of ADAR1-mediated A-to-I editing in induced pluripotent stem cell (iPSC) reprogramming.
  • To elucidate the molecular mechanisms by which ADAR1 influences cell fate transitions.

Main Methods:

  • Utilized chemical and genetic approaches to study ADAR1 function.
  • Investigated innate immune responses, endoplasmic reticulum (ER) stress, and the unfolded protein response (UPR) pathway.
  • Analyzed double-stranded RNA (dsRNA) sensing by MDA5 and its impact on membrane protein expression.

Main Results:

  • Loss of ADAR1-mediated A-to-I editing disrupts mesenchymal-to-epithelial transition (MET) during iPSC reprogramming.
  • Absence of ADAR1 triggers aberrant innate immune responses via MDA5, leading to ER stress and hindering epithelial fate.
  • A-to-I editing prevents MDA5 sensing of dsRNAs, promoting ER homeostasis and facilitating MET through the PERK-dependent UPR pathway.

Conclusions:

  • ADAR1 and its A-to-I editing activity are critical for successful cell fate transitions during reprogramming.
  • ADAR1-mediated RNA editing provides a key regulatory mechanism for MET, ensuring efficient reprogramming to pluripotency.