In addition to its classical role as a cell stress mediator, JNK, like Notch, plays roles in multiple morphogenetic processes including proliferation, cell death, and cell shape changes (Rios-Barrera and Riesgo-Escovar, 2013).
Consistent with previous results that overexpression of the small GTPase Rac1 would affect eye development, we found that expression of Rac1 under GMR promoter produced a complete eye loss phenotype, resulting from extensive cell death posterior to the morphogenetic furrow (MF) in third instar eye discs, as shown by acridine orange (AO) staining, a dye used to detect dying cells.
However, by following embryos developing in vivo and in vitro, we demonstrate that not cell death but a previously unknown morphogenetic event transforms the amorphous epiblast into a rosette of polarized cells.
We previously found that lenses lacking the Acvr1 gene, which encodes a bone morphogenetic protein (BMP) receptor, had abnormal proliferation and cell death in epithelial and cortical fiber cells.
Abundant cell death, be it phylogenetic, histogenetic or morphogenetic in nature, is a fundamental part of early development.
These morphogenetic processes are independent of both cell division and cell death (supplementary material Fig. S1A-H) (Iwaki et al., 2001; Lengyel and Iwaki, 2002).
These data can also be linked to previous studies showing that mouse lenses lacking the bone morphogenetic protein receptor Acvr1 have increased epithelial and cortical fiber cell death.
As reported previously [ 12], ectopic expression of a weak UAS-Egr transgene (UAS-Egrw) driven by GMR-Gal4 induced mild cell death in eye discs posterior to the morphogenetic furrow (MF), as revealed by AO staining).
Digit individualization is the oldest model of programmed cell death in vertebrates and is considered the classical morphogenetic example for how programmed cell death sculpts an organ (recently reviewed in Hernandez-Martinez et al. The very restricted cell death pattern in the developing limb suggests that the degeneration of a preformed interdigital tissue is required to free the digits.
Initial insight into the cellular mechanism underlying this morphogenetic movement came from the mis-rotation phenotypes observed in certain cell death mutants, such as hid.
This effect on cell death can also be induced by expression of the bone morphogenetic protein (BMP) family: Msx2 and p21 are induced following BMP4 treatment, and both molecules are necessary for BMP4-mediated cell death to occur in several cell types [ 21, 22].
