Abstract
The precise coordination of cell death and cell differentiation during the formation of developing digits is essential for generating properly shaped limbs. Retinoic acid (RA) has a fundamental role in digit development; it promotes or inhibits the molecular expression of several critical genes. This control of gene expression establishes molecular cascades that enable both the commencement of cell death and the inhibition of cell differentiation. In this review, we focus on the antagonistic functions between RA and fibroblast growth factor (FGF) signaling in the control of cell death and between RA and transforming growth factor beta (TGFβ) signaling in the control of cell differentiation.
Highlights
During formation of definitively shaped embryonic limbs, molecular control of cell differentiation and death directs the number of digits and digit separation
In embryonic chick limbs, Transforming Growth Factor beta (TGFβ)/activin signaling promotes cartilage differentiation and interdigital cell death has been shown to depend on retinoic acid (RA)
Studies on rodents fed with a Vitamin A-deficient (VAD) diet showed that many organ systems were negatively affected, which reflects the importance of Retinoic acid (RA) during embryonic development [52,53]
Summary
During formation of definitively shaped embryonic limbs, molecular control of cell differentiation and death directs the number of digits and digit separation. In species with free digits, cell death occurs in the interdigital tissue. In species with webbed digits, interdigital membranes are permanent, because the molecular cascades responsible for cell death are inhibited. At advanced stages of limb development, cells from the undifferentiated zone underneath the apical ectodermal ridge (AER) either differentiate or die, according to signals that they receive once they move away from the zone [1]. In embryonic chick limbs, Transforming Growth Factor beta (TGFβ)/activin signaling promotes cartilage differentiation and interdigital cell death has been shown to depend on retinoic acid (RA). The main aim of this review is to summarize the current knowledge on the molecular control of programmed cell death by RA during digit development
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