Early regulative ability of the neuroepithelium to form cardiac neural crest

Abstract

The cardiac neural crest (arising from the level of hindbrain rhombomeres 6–8) contributes to the septation of the cardiac outflow tract and the formation of aortic arches. Removal of this population after neural tube closure results in severe septation defects in the chick, reminiscent of human birth defects. Because neural crest cells from other axial levels have regenerative capacity, we asked whether the cardiac neural crest might also regenerate at early stages in a manner that declines with time. Accordingly, we find that ablation of presumptive cardiac crest at stage 7, as the neural folds elevate, results in reformation of migrating cardiac neural crest by stage 13. Fate mapping reveals that the new population derives largely from the neuroepithelium ventral and rostral to the ablation. The stage of ablation dictates the competence of residual tissue to regulate and regenerate, as this capacity is lost by stage 9, consistent with previous reports. These findings suggest that there is a temporal window during which the presumptive cardiac neural crest has the capacity to regulate and regenerate, but this regenerative ability is lost earlier than in other neural crest populations.

Misregulation of SDF1-CXCR4 Signaling Impairs Early Cardiac Neural Crest Cell Migration Leading to Conotruncal Defects

“…However, this model fits with the recent observations that cardiac NCs can only regenerate and repopulate the heart region when ablated before HH9 and not later. 33 Indeed, at this early stage, Sdf1 is still expressed in the ectoderm and is, therefore, able to attract the regenerating NCs expressing CXCR4.…”

Seq Your Destiny: Neural Crest Fate Determination in the Genomic Era

“…While many of the enriched transcription factors were shared with the cranial neural crest (138), one transcription factor, Tgif1, was specifically expressed in the delaminating cardiac neural crest in the dorsal hindbrain. This was particularly interesting since its expression correlates with the time at which the neural crest cells from this axial level become restricted to a cardiac fate (39). Loss of Tgif1 resulted in a downregulation of cardiac neural crest markers without affecting the expression of pan-neural crest genes.…”

Wnt Signaling in Neural Crest Ontogenesis and Oncogenesis

“…The vagal NC forms various cell types in thymus, thyroid, parathyroid, and heart; and also forms ganglia in lung, pancreas, and the gut [13]. Cardiac NC cells arise from the dorsal neural tube between the otic vesicle and the third somite in the vagal crest segment [13,14]. These cells are required in avians to trigger restructuring of the developing cardiac outflow tract [15].…”