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#dorsal-ventral axis

8 public questions tagged with this topic.

Which transcription factor is essential for specifying neural tube patterning along the dorsal-ventral axis?

Ventral neural tube patterning relies on Sonic hedgehog morphogen interpreted through Gli transcription factors, particularly Gli2 activator and Gli3 repressor forms, to establish nested expression of homeodomain proteins forming progenitor code. Shh gradient represses Class I factors Pax6, Dbx1, Irx3 ventrally and induces Class II factors Nkx2.2, Olig2, Nkx6.1 in threshold-dependent manner. Cross-repressive interactions between classes sharpen boundaries creating five ventral progenitor domains that generate distinct interneuron and motor neuron subtypes essential for circuitry. Sox2 maintains neural progenitors, Nanog and Oct4 regulate pluripotency not dorsoventral patterning. Therefore Shh signaling through Gli is central specifier.

Ref: Briscoe and Small, Development 2015, Shh-Gli Code in Neural Tube Patterning.

Which signaling molecule is responsible for specifying neural tube patterning along the dorsal-ventral axis?

Ventral neural tube identity is controlled by Sonic hedgehog secreted from notochord and floor plate. Shh diffuses dorsally establishing a ventral-to-dorsal gradient that antagonizes dorsal BMP and Wnt signals from roof plate. Different thresholds activate graded transcription factor codes: high Shh induces Nkx2.2 and floor plate genes, intermediate induces Olig2 and motor neurons, low induces Pax6 and interneurons. Gli activator-repressor ratio translates Shh dose into position-specific gene expression, compartmentalizing motor neuron, V0-V3 interneuron domains along dorsoventral axis essential for functional spinal cord circuitry and locomotor output.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 13: Neural Tube Dorsoventral Patterning by Shh.

Which of the following determines the dorsal-ventral axis in C. elegans?

Dorsal-ventral axis in C. elegans originates from early cell contacts rather than diffusible gradients like BMP in vertebrates. At four-cell embryo, AB and P1 touching geometry differentially positions ABp contacting P2 receiving GLP-1 Notch signal involving APX-1, while ABa does not contact P2. This differential contact plus SKN-1, PAR polarity cues orients mitotic spindles via GPR-1/2 G-alpha regulation, positioning descendants dorsally versus ventrally. Physical interaction between AB derivatives and P1 lineage mediated by cadherin HMR-1 and catenin HMP-1 translates contact asymmetry into fate segregation essential for nervous system positioning.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: AB-P1 interaction establishes dorsal-ventral axis via Notch.

Which molecule establishes the dorsal-ventral axis of the limb?

Dorsal-ventral polarity originates from ectoderm-mesenchyme signaling interactions conserved across vertebrates and mammals. Dorsal ectoderm secretes Wnt7a, which via canonical beta-catenin pathway induces LIM-homeodomain factor Lmx1b in underlying dorsal mesenchyme, conferring dorsal character to skin, nails, sesamoids and extensor musculature. Ventral ectoderm expresses Engrailed-1, which represses Wnt7a, confining it dorsally and permitting ventral BMP-driven fate with thick volar pads. Loss of Wnt7a ventralizes dorsal limb causing biventral double-ventral phenotype. TBX5 specifies forelimb, Lmx1b executes dorsal program downstream, RA patterns proximal-distal axis.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: Wnt7a establishment of dorsal-ventral limb axis.

The initial dorsal-ventral axis in amphibian embryos is determined by:

Amphibian dorsoventral axis established immediately after fertilization by sperm-induced cortical rotation. Sperm centriole nucleates microtubule array that transports dorsal determinants Dishevelled and GBP with plus-end kinesins to side opposite sperm entry, defining dorsal gray crescent enriched with beta-catenin stabilization factors. Gravity can bias rotation but primary cue is sperm entry point triggering cytoskeletal rearrangement. Genetic programs downstream including Wnt and Nodal refine axis but initial asymmetry derives from sperm entry triggering rotation rather than purely genetic preformation or blastocoel formation random position, linking fertilization site to organizer formation.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 8: Dorsal-ventral axis determination by point of sperm entry.

Chick embryo dorsal-ventral axis initially depends on:

Early avian dorsal-ventral polarity before gastrulation linked to bioelectric patterns across blastoderm. Measurements show potential difference and intracellular pH gradient between dorsal epiblast and ventral hypoblast established during egg rotation in oviduct, mediated by ion transporters H+ V-ATPase and Na+/K+ ATPase. Depolarization of embryonic side elevates beta-catenin. Gravity and primitive streak act later. Experimental equalization of membrane potential ventralizes embryos. Therefore initial dorsal-ventral axis depends on egg membrane potential and pH differences rather than solely gravity or primitive streak itself. This illustrates conserved developmental logic of morphogen gradients patterning embryonic axes through Wnt and BMP antagonism.

Ref: Stern, Gastrulation in avian embryos - Bioelectric cues for dorsal-ventral axis, Developmental Biology.

Initial dorsal-ventral axis in amphibians is set by:

Initial breaking of radial symmetry in amphibians occurs at fertilization when sperm aster forms in vegetal cortex. Astral microtubules guide cortical rotation moving dorsal determinants 30 degrees away from sperm entry point. Sperm entry site therefore becomes ventral pole while opposite side accumulates Wnt11, Dishevelled and GBP, stabilizing beta-catenin dorsally. Gravity can bias but not determine axis; genetic differences and uterine orientation irrelevant in oviparous amphibians. Thus point of sperm entry sets dorso-ventral axis by directing cortical rotation direction and dorsal determinant transport. This illustrates conserved developmental logic of morphogen gradients patterning embryonic axes through Wnt and BMP antagonism.

Ref: Wolpert, Principles of Development, Chapter 4: Sperm entry and amphibian axis specification.

Dorsal-ventral axis in Drosophila is primarily determined by:

Dorsoventral polarity originates during oogenesis when Gurken, a TGF-alpha-like ligand, secreted from oocyte nucleus located dorsal-anterior position activates EGFR in adjacent follicle cells. Dorsal follicle fate represses Pipe sulfotransferase expression ventrally, restricting Pipe to ventral follicle cells that modify vitelline membrane. After fertilization, serine protease cascade downstream of Pipe cleaves Spätzle, activating Toll receptor ventrally. Toll signaling via Tube, Pelle degrades Cactus inhibitor, allowing Dorsal NF-kB transcription factor nuclear entry ventrally. Thus Gurken dorsalizes follicle cells and Dorsal patterns embryo ventrally, jointly establishing DV axis.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Dorsoventral patterning Gurken and Dorsal.