Developmental Signals - Six

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Introduction

Sine oculis-related homeobox (Six) is a homeobox gene family. In humans, mutations of SIX1 cause branchio-oto-renal (BOR) syndrome, an autosomal dominant disorder characterized by hearing loss, pharyngeal arch defects and various renal abnormalities.


Factor Links: AMH | hCG | BMP | sonic hedgehog | bHLH | HOX | FGF | FOX | Hippo | LIM | Nanog | NGF | Nodal | Notch | PAX | retinoic acid | SIX | Slit2/Robo1 | SOX | TBX | TGF-beta | VEGF | WNT | Category:Molecular

Some Recent Findings

  • Mice doubly deficient in Six4 and Six5 show ventral body wall defects reproducing human omphalocele[1] "Omphalocele is a human congenital anomaly in ventral body wall closure and may be caused by impaired formation of the primary abdominal wall (PAW) and/or defects in abdominal muscle development. Here, we report that mice doubly deficient in homeobox genes Six4 and Six5 showed the same ventral body wall closure defects as those seen in human omphalocele. SIX4 and SIX5 were localized in surface ectodermal cells and somatic mesoderm-derived mesenchymal and coelomic epithelial cells (CECs) in the PAW." omphalocele
  • Activation of Six1 Expression in Vertebrate Sensory Neurons[2] "SIX1 homeodomain protein is one of the essential key regulators of sensory organ development. Six1-deficient mice lack the olfactory epithelium, vomeronasal organs, cochlea, vestibule and vestibuloacoustic ganglion, and also show poor neural differentiation in the distal part of the cranial ganglia. Simultaneous loss of both Six1 and Six4 leads to additional abnormalities such as small trigeminal ganglion and abnormal dorsal root ganglia (DRG)."
More recent papers  
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Search term: Development Six

<pubmed limit=5>Development Six</pubmed>

Transcription Factor

Neural Development

Vision Development

Abnormalities

omphalocele - Mice doubly deficient in Six4 and Six5 show ventral body wall defects reproducing human omphalocele [1]


References

  1. 1.0 1.1 Takahashi M, Tamura M, Sato S & Kawakami K. (2018). Mice doubly deficient in Six4 and Six5 show ventral body wall defects reproducing human omphalocele. Dis Model Mech , 11, . PMID: 30237319 DOI.
  2. Sato S, Yajima H, Furuta Y, Ikeda K & Kawakami K. (2015). Activation of Six1 Expression in Vertebrate Sensory Neurons. PLoS ONE , 10, e0136666. PMID: 26313368 DOI.

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Reviews

Articles

Sato S, Yajima H, Furuta Y, Ikeda K & Kawakami K. (2015). Activation of Six1 Expression in Vertebrate Sensory Neurons. PLoS ONE , 10, e0136666. PMID: 26313368 DOI.

Yajima H, Suzuki M, Ochi H, Ikeda K, Sato S, Yamamura K, Ogino H, Ueno N & Kawakami K. (2014). Six1 is a key regulator of the developmental and evolutionary architecture of sensory neurons in craniates. BMC Biol. , 12, 40. PMID: 24885223 DOI.

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http://www.ncbi.nlm.nih.gov/omim

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Cite this page: Hill, M.A. (2018, December 16) Embryology Developmental Signals - Six. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Signals_-_Six

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© Dr Mark Hill 2018, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G