The bHLH Factors, dHAND and eHAND, Specify Pulmonary and Systemic Cardiac Ventricles Independent of Left–Right Sidedness

Thomas, Tiffani; Yamagishi, Hiroyuki; Overbeek, Paul A.; Olson, Eric N.; Srivastava, Deepak

doi:10.1006/dbio.1998.8849

Cited by 190 publications

(127 citation statements)

References 18 publications

(17 reference statements)

Supporting

Mentioning

120

Contrasting

Unclassified

Order By: Relevance

“…The expression of eHAND has not been studied previously in relation to limb development, although it has been extensively studied in other systems such as the heart (Thomas et al, 1998a). In chick embryos, the expression of eHAND during limb bud development can be considered to evolve in three different phases.…”

Section: Discussionmentioning

confidence: 99%

Expression and regulation of eHAND during limb development

Fernandez-Teran

Piedra

Rodríguez‐Rey

et al. 2003

Developmental Dynamics

View full text Add to dashboard Cite

eHAND is a bHLH transcription factor with important functions during embryogenesis. Here, we report that eHAND has a dynamic pattern of expression during limb development. In chick embryos, eHAND expression is first observed in the ventral mesoderm of the emerging limb. Its expression is then restricted to an anteroventral area of mesoderm at mid-level in the proximodistal axis. At later stages, expression is observed in the autopod encompassing the ventral tendons of the digits. In mouse embryos, only the anteroventral domain of expression is conserved, the early ventral expression not being detectable and the late pattern of expression differing clearly from that in the chick. A constant feature of all areas of expression is their ventral and anterior localization. Respecification of the anterior mesoderm as occurs secondarily to Sonic hedgehog (SHH) or retinoic acid application to the anterior border leads to downregulation of eHAND expression. Accordingly, eHAND expression is not detectable in talpid 2 mutant limbs, which are considered to be posteriorized limbs. However, eHAND expression is little modified in oligozeugodactyly, a chick mutant that lacks Shh signaling in the limb but retains certain anteroposterior polarity. Interestingly, eHAND expression is also linked to the ventral identity of the mesoderm and is repressed by the dorsal ectoderm. It is also positively regulated by bone morphogenetic protein signaling, which is also known to participate in dorsoventral patterning. We suggest that eHAND expression may be related to the anteroventral identity of the mesoderm. However, in overexpression experiments using retroviral vectors, only a low percentage of cases (5%) showed phenotypic alterations, consisting of a duplication of digit 2. Developmental Dynamics 226:690 -701, 2003.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression and regulation of eHAND during limb development

Fernandez-Teran

Piedra

Rodríguez‐Rey

et al. 2003

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…Their expression, however, arises during the looping event, i.e., rather reflect anterior-posterior pattering, but not regulation by the L/R pathway (Thomas et al, 1998). Observation of asymmetric gene expression, especially in the heart, thus is not sufficient to deduce an involvement in the development of laterality.…”

Section: Galanin and Lr Asymmetrymentioning

confidence: 94%

“…Other genes such as eHand, dHand, or Shox2 are transcribed asymmetrically in the four-chambered heart (Thomas et al, 1998;Blaschke et al, 2007). Their expression, however, arises during the looping event, i.e., rather reflect anterior-posterior pattering, but not regulation by the L/R pathway (Thomas et al, 1998).…”

Section: Galanin and Lr Asymmetrymentioning

confidence: 99%

Left‐asymmetric expression of Galanin in the linear heart tube of the mouse embryo is independent of the nodal co‐receptor gene cryptic

Schweickert

Deißler

Britsch

et al. 2008

Developmental Dynamics

View full text Add to dashboard Cite

Only very few left/right asymmetrically expressed genes are known in the mammalian embryo. In a screen for novel factors we identified the gene encoding the neuropeptide Galanin in mouse. At embryonic day (E) 8.5 asymmetric mRNA transcription was found in the left half of the linear heart tube. During heart looping and morphogenesis expression became restricted to the atrio-ventricular (AV) canal, followed by specific staining of the AV-node and AV-rings in the four-chambered heart. Expression was inverted in inv/inv and randomized in homozygous iv mutant embryos. Left-sided heart-specific transcription of mouse Gal thus should be controlled by the left-right pathway. The asymmetric pattern was retained in cryptic mutant embryos, in which the Nodal signaling cascade is disrupted. Surprisingly, Pitx2c was found to be expressed in 50% of cryptic mutant hearts as well, suggesting that some aspects of asymmetric gene expression in the heart are independent of cryptic. Developmental Dynamics 237:3557-3564, 2008.

show abstract

“…Embryos were collected on the indicated days postconception and fixed in 4% paraformaldehyde for 24 to 48 h. Embryos were dehydrated through a series of ethanol solutions and embedded in paraffin. In situ hybridization with the eHAND probe was performed as previously described (36,37). In situ hybridization slides were photographed on a Nikon E600 microscope with fluorescent lighting using darkfield imaging with a red filter (Nikon, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

PIP5KIγ is required for cardiovascular and neuronal development

Wang

Lian²,

Golden³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

All eukaryotic cells contain the phospholipid phosphatidylinositol 4, 5-bisphosphate (PIP2) that serves multiple roles in signal transduction cascades. Type I phosphatidylinositol-4-phosphate 5-kinase (PIP5KI) catalyzes the synthesis of PIP2 by phosphorylating phosphatidylinositol 4 phosphate. Although the classical isoforms of PIP5KI (designated as ␣, ␤, and ␥) all generate the same phospholipid product, they have significantly dissimilar primary structures and expression levels in different tissues, and they appear to localize within different compartments within the cell. Therefore, it appears likely that PIP5KI isoforms have overlapping, but not identical, functions. Here we show that targeted disruption of PIP5KI␥ causes widespread developmental and cellular defects. PIP5KI␥-null embryos have myocardial developmental defects associated with impaired intracellular junctions that lead to heart failure and extensive prenatal lethality at embryonic day 11.5 of development. Loss of PIP5KI␥ also results in neural tube closure defects that were associated with impaired PIP2 production, adhesion junction formation, and neuronal cell migration. These data, along with those of other PIP5KI isoforms, indicate that individual PIP5KI isoenzymes fulfill specific roles in embryonic development.phosphoinositide ͉ phospholipid ͉ phosphatidylinositol 4,5-bisphosphate

show abstract

The bHLH Factors, dHAND and eHAND, Specify Pulmonary and Systemic Cardiac Ventricles Independent of Left–Right Sidedness

Cited by 190 publications

References 18 publications

Expression and regulation of eHAND during limb development

Expression and regulation of eHAND during limb development

Left‐asymmetric expression of Galanin in the linear heart tube of the mouse embryo is independent of the nodal co‐receptor gene cryptic

PIP5KIγ is required for cardiovascular and neuronal development

Contact Info

Product

Resources

About