PMID- 10529420
OWN - NLM
STAT- MEDLINE
DCOM- 19991217
LR  - 20220225
IS  - 0950-1991 (Print)
IS  - 0950-1991 (Linking)
VI  - 126
IP  - 22
DP  - 1999 Nov
TI  - Mice mutant for both Hoxa1 and Hoxb1 show extensive remodeling of the hindbrain
      and defects in craniofacial development.
PG  - 5027-40
AB  - The analysis of mice mutant for both Hoxa1 and Hoxb1 suggests that these two
      genes function together to pattern the hindbrain. Separately, mutations in Hoxa1 
      and Hoxb1 have profoundly different effects on hindbrain development. Hoxa1
      mutations disrupt the rhombomeric organization of the hindbrain, whereas Hoxb1
      mutations do not alter the rhombomeric pattern, but instead influence the fate of
      cells originating in rhombomere 4. We suggest that these differences are not the 
      consequences of different functional roles for these gene products, but rather
      reflect differences in the kinetics of Hoxa1 and Hoxb1 gene expression. In strong
      support of the idea that Hoxa1 and Hoxb1 have overlapping functions, Hoxa1/Hoxb1 
      double mutant homozygotes exhibit a plethora of defects either not seen, or seen 
      only in a very mild form, in mice mutant for only Hoxa1 or Hoxb1. Examples
      include: the loss of both rhombomeres 4 and 5, the selective loss of the 2(nd)
      branchial arch, and the loss of most, but not all, 2(nd) branchial arch-derived
      tissues. We suggest that the early role for both of these genes in hindbrain
      development is specification of rhombomere identities and that the aberrant
      development of the hindbrain in Hoxa1/Hoxb1 double mutants proceeds through two
      phases, the misspecification of rhombomeres within the hindbrain, followed
      subsequently by size regulation of the misspecified hindbrain through induction
      of apoptosis.
FAU - Rossel, M
AU  - Rossel M
AD  - Howard Hughes Medical Institute, Department of Human Genetics, University of Utah
      School of Medicine, Salt Lake City, Utah 84112, USA.
FAU - Capecchi, M R
AU  - Capecchi MR
LA  - eng
GR  - HD-6-2915/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Development
JT  - Development (Cambridge, England)
JID - 8701744
RN  - 0 (Avian Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Early Growth Response Protein 2)
RN  - 0 (Egr2 protein, mouse)
RN  - 0 (Fetal Proteins)
RN  - 0 (HOXB1 homeodomain protein)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (Hoxb2 protein, mouse)
RN  - 0 (MafB Transcription Factor)
RN  - 0 (Mafb protein, mouse)
RN  - 0 (Oncogene Proteins)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Transcription Factor AP-2)
RN  - 0 (Transcription Factors)
RN  - 0 (homeobox A1 protein)
RN  - 0 (retinoic acid binding protein I, cellular)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, EphA4)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - *Avian Proteins
MH  - Branchial Region/abnormalities/embryology
MH  - Craniofacial Abnormalities/*genetics/pathology
MH  - DNA-Binding Proteins/biosynthesis
MH  - Early Growth Response Protein 2
MH  - Embryonic and Fetal Development
MH  - Fetal Proteins/biosynthesis
MH  - Genotype
MH  - Homeodomain Proteins/biosynthesis/*genetics
MH  - MafB Transcription Factor
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Motor Neurons/physiology
MH  - Mutation
MH  - *Oncogene Proteins
MH  - Receptor Protein-Tyrosine Kinases/biosynthesis
MH  - Receptor, EphA4
MH  - Receptors, Retinoic Acid/biosynthesis
MH  - Rhombencephalon/abnormalities/*embryology/pathology
MH  - Transcription Factor AP-2
MH  - Transcription Factors/biosynthesis/*genetics
EDAT- 1999/10/26 00:00
MHDA- 1999/10/26 00:01
CRDT- 1999/10/26 00:00
PHST- 1999/10/26 00:00 [pubmed]
PHST- 1999/10/26 00:01 [medline]
PHST- 1999/10/26 00:00 [entrez]
AID - 10.1242/dev.126.22.5027 [doi]
PST - ppublish
SO  - Development. 1999 Nov;126(22):5027-40. doi: 10.1242/dev.126.22.5027.