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#lateral plate mesoderm

2 public questions tagged with this topic.

Which signaling molecule stabilizes hindlimb formation in lateral plate mesoderm?

Hindlimb field positioning and maintenance require Wnt8c signaling in caudal lateral plate mesoderm acting upstream of FGF10. Wnt8c activates canonical beta-catenin cascade inducing and stabilizing FGF10 transcription and supporting Islet1 Pitx1 expression, analogous to Wnt3 requirement anteriorly for forelimb initiation. Wnt8c expression colocalizes with forming hindlimb bud mesenchyme, preceding FGF10 upregulation and marking hindlimb competence. Wnt3a induces AER via beta-catenin primarily in forelimb region, beta-catenin common mediator, RA influences proximal-distal patterning rather than hindlimb stabilization. Thus Wnt8c anchors hindlimb formation and prevents regression.

Ref: Kawakami et al., Development, Gilbert Chapter 20: Wnt8c stabilization of hindlimb mesoderm.

What happens when Islet1 is knocked out in the lateral plate mesoderm?

Hindlimb field specification requires LIM-homeodomain transcription factor Islet1 in posterior lateral plate mesoderm. Islet1 promotes nuclear accumulation of beta-catenin activating beta-catenin pathway and directly drives Fgf10 expression initiating hindlimb bud. Early inactivation of Islet1 via conditional deletion in lateral plate leads to failure of Fgf10-Fgf8 feedback establishment selectively in hindlimb, resulting in complete hindlimb agenesis while forelimbs remain intact. It also regulates Hand2-Shh pathway posteriorly. Therefore Islet1 acts as hindlimb-specific initiator upstream of beta-catenin and represents missing regulatory link distinguishing hindlimb from forelimb.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 19: Islet1 in hindlimb initiation and beta-catenin activation pathway.