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Atoh1 governs the migration of postmitotic neurons that shape respiratory effectiveness at birth and chemoresponsiveness in adulthood.

Hindbrain neuronal networks serving respiratory, proprioceptive, and arousal functions share a developmental requirement for the bHLH transcription factor Atoh1. Loss of Atoh1 in mice results in respiratory failure and neonatal lethality; however, the neuronal identity and mechanism by which Atoh1-dependent cells sustain newborn breathing remains unknown. We uncovered that selective loss of Atoh1 from the postmitotic retrotrapezoid nucleus (RTN) neurons results in severely impaired inspiratory rhythm and pronounced neonatal death. Mice that escape neonatal death develop abnormal chemoresponsiveness as adults. Interestingly, the expression of Atoh1 in the RTN neurons is not required for their specification or maintenance, but is important for their proper localization and to establish essential connections with the preBötzinger Complex (preBötC). These results provide insights into the genetic regulation of neonatal breathing and shed light on the labile sites that might contribute to sudden death in newborn infants and altered chemoresponsiveness in adults.

Pubmed ID: 22958821


  • Huang WH
  • Tupal S
  • Huang TW
  • Ward CS
  • Neul JL
  • Klisch TJ
  • Gray PA
  • Zoghbi HY



Publication Data

September 6, 2012

Associated Grants

  • Agency: NICHD NIH HHS, Id: HD24064
  • Agency: NICHD NIH HHS, Id: P30 HD024064
  • Agency: NICHD NIH HHS, Id: R01 HD062553
  • Agency: NHLBI NIH HHS, Id: R01 HL089742
  • Agency: NHLBI NIH HHS, Id: R01HL089742
  • Agency: Howard Hughes Medical Institute, Id:
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Age Factors
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Movement
  • Disease Models, Animal
  • Female
  • Humans
  • Infant, Newborn
  • Male
  • Mice
  • Mice, Knockout
  • Pregnancy
  • Respiratory Center
  • Respiratory Physiological Phenomena
  • Rhombencephalon