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#dorsal-ventral polarity

2 public questions tagged with this topic.

Which gene is expressed in the dorsal ectoderm and controls limb dorsal-ventral polarity?

Dorsal-ventral limb polarity originates from non-AER ectodermal signals rather than ridge. Wnt7a transcript localized specifically to dorsal ectoderm induces LIM homeodomain transcription factor Lmx1b in dorsal mesoderm, conferring dorsal characteristics including nails, dorsal tendon pattern, hair orientation and pigmentation. Ventral ectoderm expresses Engrailed1 repressing Wnt7a and activating BMP signaling promoting ventral fates like footpads. Ectoderm rotation experiments inverting DV orientation produce inverted limb polarity, confirming ectodermal instruction. Wnt7a also contributes to maintaining SHH posteriorly, integrating axes, but primary function remains dorsalizing mesenchyme through Lmx1b induction pathway.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 19: Wnt7a dorsal ectoderm and Lmx1b dorsalization of mesoderm.

Dorsal-ventral polarity in Drosophila is initially set by:

Dorsal-ventral axis in Drosophila originates during oogenesis when Gurken mRNA localized to oocyte antero-dorsal cortex translates into TGF-alpha-like ligand activating Torpedo/EGFR in adjacent follicular epithelium. EGFR signaling represses transcription of sulfotransferase Pipe to ventral side, creating ventral domain where Pipe modifies vitelline membrane proteins. This modification permits serine protease cascade involving Nudel, Gastrulation defective, Snake, Easter that cleaves Spatzle ventrally. Processed Spatzle activates Toll uniformly present in embryonic membrane, generating ventral nuclear gradient of Dorsal transcription factor. Therefore initial polarity derives from Gurken-Torpedo communication between germline and somatic follicle cells rather than downstream Toll or Easter alone.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 9: Gurken-Torpedo EGFR signaling setting follicular DV polarity.