PMID- 10625552
OWN - NLM
STAT- MEDLINE
DCOM- 20000210
LR  - 20161124
IS  - 0012-1606 (Print)
IS  - 0012-1606 (Linking)
VI  - 217
IP  - 2
DP  - 2000 Jan 15
TI  - Cardiac expression of the ventricle-specific homeobox gene Irx4 is modulated by
      Nkx2-5 and dHand.
PG  - 266-77
AB  - We report the isolation and characterization of the cDNAs encoded by the murine
      and human homeobox genes, Irx4 (Iroquois homeobox gene 4). Mouse and human Irx4
      proteins are highly conserved (83%) and their 63-aa homeodomain is more than 93% 
      identical to that of the Drosophila Iroquois patterning genes. Human IRX4 maps to
      chromosome 5p15.3, which is syntenic to murine chromosome 13. Irx4 transcripts
      are present in the developing central nervous system, skin, and vibrissae, but
      are predominantly expressed in the cardiac ventricles. In mice at embryonic day
      (E) 7.5, Irx4 transcripts are found in the chorion and at low levels in a
      discrete anterior domain of the cardiac primordia. During the formation of the
      linear heart tube and its subsequent looping (E8.0-8.5), Irx4 expression is
      restricted to the ventricular segment and is absent from both the posterior
      (eventual atrial) and the anterior (eventual outflow tract) segments of the
      heart. Throughout all subsequent stages in which the chambers of the heart become
      morphologically distinct (E8.5-11) and into adulthood, cardiac Irx4 expression is
      found exclusively in the ventricular myocardium. Irx4 gene expression was also
      assessed in embryos with aberrant cardiac development: mice lacking RXRalpha or
      MEF2c have normal Irx4 expression, but mice lacking the homeobox transcription
      factor Nkx2-5 (Csx) have markedly reduced levels of Irx4 transcripts. dHand-null 
      embryos initiate Irx4 expression, but cannot maintain normal levels. These data
      indicate that the homeobox gene Irx4 is likely to be an important mediator of
      ventricular differentiation during cardiac development, which is downstream of
      Nkx2-5 and dHand.
CI  - Copyright 2000 Academic Press.
FAU - Bruneau, B G
AU  - Bruneau BG
AD  - Department of Genetics, Harvard Medical School, Boston, Massachusetts, 02115,
      USA.
FAU - Bao, Z Z
AU  - Bao ZZ
FAU - Tanaka, M
AU  - Tanaka M
FAU - Schott, J J
AU  - Schott JJ
FAU - Izumo, S
AU  - Izumo S
FAU - Cepko, C L
AU  - Cepko CL
FAU - Seidman, J G
AU  - Seidman JG
FAU - Seidman, C E
AU  - Seidman CE
LA  - eng
SI  - GENBANK/AF124732
SI  - GENBANK/AF124733
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Dev Biol
JT  - Developmental biology
JID - 0372762
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (HAND2 protein, human)
RN  - 0 (Hand2 protein, mouse)
RN  - 0 (Homeobox Protein Nkx-2.5)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (IRX4 protein, human)
RN  - 0 (Irx4 protein, Xenopus)
RN  - 0 (Irx4 protein, mouse)
RN  - 0 (NKX2-5 protein, human)
RN  - 0 (Nkx2-5 protein, mouse)
RN  - 0 (Transcription Factors)
RN  - 0 (Xenopus Proteins)
RN  - 0 (Zebrafish Proteins)
RN  - 0 (hand2 protein, zebrafish)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Basic Helix-Loop-Helix Transcription Factors
MH  - Cloning, Molecular
MH  - Conserved Sequence
MH  - DNA-Binding Proteins/*metabolism
MH  - Evolution, Molecular
MH  - Heart Defects, Congenital/genetics
MH  - Heart Ventricles/*embryology
MH  - Homeobox Protein Nkx-2.5
MH  - Homeodomain Proteins/genetics/*metabolism
MH  - Humans
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Molecular Sequence Data
MH  - Sequence Homology, Amino Acid
MH  - Transcription Factors/*metabolism
MH  - *Xenopus Proteins
MH  - Zebrafish Proteins
EDAT- 2000/01/08 00:00
MHDA- 2000/01/08 00:01
CRDT- 2000/01/08 00:00
PHST- 2000/01/08 00:00 [pubmed]
PHST- 2000/01/08 00:01 [medline]
PHST- 2000/01/08 00:00 [entrez]
AID - 10.1006/dbio.1999.9548 [doi]
AID - S0012-1606(99)99548-9 [pii]
PST - ppublish
SO  - Dev Biol. 2000 Jan 15;217(2):266-77. doi: 10.1006/dbio.1999.9548.