Vitamin A-deficient quail embryos have half a hindbrain and other neural defects

Maden, Malcolm; Gale, Emily; Kostetskii, Igor; Zile, Maija H.

doi:10.1016/s0960-9822(02)00509-2

Cited by 316 publications

(204 citation statements)

References 60 publications

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“…Such a loss of the postotic neural crest stream is also observed in VAD quail embryos (Maden et al, 1996). Labeling with rhombomerespecific markers shows that the rhombomeres posterior to r4 are not specified when RA is blocked during gastrulation in either the zebrafish or in VAD quail embryos ( Fig.…”

Section: Loss Of Ra During Gastrulation Causes Neural Crest Defects mentioning

confidence: 65%

Retinoic acid is required for endodermal pouch morphogenesis and not for pharyngeal endoderm specification

Kopinke

Sasine

Swift

et al. 2006

Developmental Dynamics

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Because tissues from all three germ layers contribute to the pharyngeal arches, it is not surprising that all major signaling pathways are involved in their development. We focus on the role of retinoic acid (RA) signaling because it has been recognized for quite some time that alterations in this pathway lead to craniofacial malformations. Several studies exist that describe phenotypes observed upon RA perturbations in pharyngeal arch development; however, these studies did not address whether RA plays multiple roles at distinct time points during development. Here, we report the resulting phenotypes in the hindbrain, the neural crest-derived tissues, and the pharyngeal endoderm when RA synthesis is disrupted during zebrafish gastrulation and pharyngeal arch morphogenesis. Our results demonstrate that RA is required for the postgastrulation morphogenesis and segmentation of endodermal pouches, and that loss of RA does not affect the length of the pharyngeal ectoderm or medial endoderm along the anterior-posterior axis. We also provide evidence that RA is not required for the specification of pharyngeal pouch endoderm and that the pharyngeal endoderm consists of at least two different cell populations, of which the pouch endoderm is sensitive to RA and the more medial pharyngeal endoderm is not. These results demonstrate that the developmental processes underlying pharyngeal arch defects differ depending on when RA signaling is disturbed during development.

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Section: Loss Of Ra During Gastrulation Causes Neural Crest Defects mentioning

confidence: 65%

Retinoic acid is required for endodermal pouch morphogenesis and not for pharyngeal endoderm specification

Kopinke

Sasine

Swift

et al. 2006

Developmental Dynamics

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“…In the hindbrain, RA is essential for the establishment of the anterior-posterior pattern, as demonstrated by embryos in which RA is depleted either dietarily, pharmacologically or genetically (Begemann et al, 2004;Dupe and Lumsden, 2001;Maden et al, 1996;Niederreither et al, 1999). RA is produced in the anterior paraxial mesoderm by the activity of aldehyde dehydrogenase 1 family, member A2 (Aldh1a2), which oxidizes retinal to RA (Begemann et al, 2001;Gavalas, 2002;Niederreither et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Cyp26 enzymes generate the retinoic acid response pattern necessary for hindbrain development

et al. 2007

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Retinoic acid (RA) is essential for normal vertebrate development,including the patterning of the central nervous system. During early embryogenesis, RA is produced in the trunk mesoderm through the metabolism of vitamin A derived from the maternal diet and behaves as a morphogen in the developing hindbrain where it specifies nested domains of Hox gene expression. The loss of endogenous sources of RA can be rescued by treatment with a uniform concentration of exogenous RA, indicating that domains of RA responsiveness can be shaped by mechanisms other than the simple diffusion of RA from a localized posterior source. Here, we show that the cytochrome p450 enzymes of the Cyp26 class, which metabolize RA into polar derivatives,function redundantly to shape RA-dependent gene-expression domains during hindbrain development. In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain. Furthermore,we show that Cyp26 enzymes are essential for exogenous RA to rescue hindbrain patterning in RA-depleted embryos. We present a `gradient-free' model for hindbrain patterning in which differential RA responsiveness along the hindbrain anterior-posterior axis is shaped primarily by the dynamic expression of RA-degrading enzymes.

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“…Retinoic acid (RA) secreted from posterior mesoderm regulates Hox gene expression in the hindbrain. Treatment of embryos with exogenous RA, or conditions that disrupt RA signaling, result in changes in Hox gene expression and fundamental changes in hindbrain patterning (Papalopulu et al, 1991;Marshall et al, 1992;Simeone et al, 1995;Alexandre et al, 1996;Maden et al, 1996;Dupe et al, 1999;Niederreither et al, 2000;White et al, 2000). Several other segmentation genes, Krox20,vhnf1,and Kreisler/valentino (mafB), regulate even earlier stages of hindbrain segmentation and are required for normal activation of various Hox genes (Sham et al, 1993;Nonchev et al, 1996;Manzanares et al, 1997Manzanares et al, , 1999Prince et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Rhombomere boundaries are Wnt signaling centers that regulate metameric patterning in the zebrafish hindbrain

Riley

Chiang

Storch

et al. 2004

Developmental Dynamics

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The vertebrate hindbrain develops from a series of segments (rhombomeres) distributed along the anteroposterior axis. We are studying the roles of Wnt and Delta-Notch signaling in maintaining rhombomere boundaries as organizing centers in the zebrafish hindbrain. Several wnt genes (wnt1, wnt3a, wnt8b, and wnt10b) show elevated expression at rhombomere boundaries, whereas several delta genes (dlA, dlB, and dlD) are expressed in transverse stripes flanking rhombomere boundaries. Partial disruption of Wnt signaling by knockdown of multiple wnt genes, or the Wnt mediator tcf3b, ablates boundaries and associated cell types. Expression of dlA is chaotic, and cell types associated with rhombomere centers are disorganized. Similar patterning defects are observed in segmentation mutants spiel-ohne-grenzen (spg) and valentino (val), which fail to form rhombomere boundaries due to faulty interactions between adjacent rhombomeres. Stripes of wnt expression are variably disrupted, with corresponding disturbances in metameric patterning. Mutations in dlA or mind bomb (mib) disrupt Delta-Notch signaling and cause a wide range of patterning defects in the hindbrain. Stripes of wnt1 are initially normal but subsequently dissipate, and metameric patterning becomes increasingly disorganized. Driving wnt1 expression using a heat-shock construct partially rescues metameric patterning in mib mutants. Thus, rhombomere boundaries act as Wnt signaling centers required for precise metameric patterning, and Delta signals from flanking cells provide feedback to maintain wnt expression at boundaries. Similar feedback mechanisms operate in the Drosophila wing disc and vertebrate limb bud, suggesting coaptation of a conserved signaling module that spatially organizes cells in complex organ systems.

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Vitamin A-deficient quail embryos have half a hindbrain and other neural defects

Abstract: These results demonstrate at least three roles for RA in central nervous system development: neural crest survival, neurite outgrowth and hindbrain patterning.

Cited by 316 publications

References 60 publications

Retinoic acid is required for endodermal pouch morphogenesis and not for pharyngeal endoderm specification

Retinoic acid is required for endodermal pouch morphogenesis and not for pharyngeal endoderm specification

Cyp26 enzymes generate the retinoic acid response pattern necessary for hindbrain development

Rhombomere boundaries are Wnt signaling centers that regulate metameric patterning in the zebrafish hindbrain

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