Specification of the anterior hindbrain and establishment of a normal mid/hindbrain organizer is dependent on Gbx2 gene function
Citations Over TimeTop 10% of 1997 papers
Abstract
Analysis of mouse embryos homozygous for a loss-of-function allele of Gbx2 demonstrates that this homeobox gene is required for normal development of the mid/hindbrain region. Gbx2 function appears to be necessary at the neural plate stage for the correct specification and normal proliferation or survival of anterior hindbrain precursors. It is also required to maintain normal patterns of expression at the mid/hindbrain boundary of Fgf8 and Wnt1, genes that encode signaling molecules thought to be key components of the mid/hindbrain (isthmic) organizer. In the absence of Gbx2 function, isthmic nuclei, the cerebellum, motor nerve V, and other derivatives of rhombomeres 1-3 fail to form. Additionally, the posterior midbrain in the mutant embryos appears to be extended caudally and displays abnormalities in anterior/posterior patterning. The failure of anterior hindbrain development is presumably due to the loss of Gbx2 function in the precursors of the anterior hindbrain. However, since Gbx2 expression is not detected in the midbrain it seems likely that the defects in midbrain anterior/posterior patterning result from an abnormal isthmic signaling center. These data provide genetic evidence for a link between patterning of the anterior hindbrain and the establishment of the mid/hindbrain organizer, and identify Gbx2 as a gene required for these processes to occur normally.
Related Papers
- → Hindbrain Neurons as an Essential Hub in the Neuroanatomically Distributed Control of Energy Balance(2012)473 cited
- → Constructing the hindbrain: Insights from the zebrafish(2002)221 cited
- → Integration Between the Epibranchial Placodes and the Hindbrain(2001)111 cited
- → ArRAnging the hindbrain(2002)77 cited
- → Model Organisms Inform the Search for the Genes and Developmental Pathology Underlying Malformations of the Human Hindbrain(2009)9 cited