TY  - JOUR
TI  - Development and programed cell death in the mammalian eye
AU  - Vecino, Elena
AU  - Acera, Arantxa
T2  - The International Journal of Developmental Biology
AB  - Programmed cell death (PCD) is a major mechanism for patterning of a variety of complex structures. Cells are initially organized into fairly loose patterns; then, selective death removes the cells between pattern elements to create the correct structures, as a sculptor removes some material to reveal the hidden image. The life or death of a cell is mostly affected by extracellular signals because the intracellular machinery responsible for PCD is constitutively expressed in most animal cells. The optic vesicle originates during gastrulation when the endoderm and mesoderm interact with the adjacent prospective head ectoderm to create a lens. To be formed correctly, the lens must have a precise spatial relationship with the retina. Ganglion cells are the first neurons to be differentiated in the retina. Vertical networks in the inner and outer retina are later interconnected when bipolar cells are formed and connections with ganglion cells are established. This sequential pattern of retinal circuit development is common across vertebrate species. During development of the retina, far more neurons are generated than are ultimately needed with almost one half of them undergoing PCD shortly before establishing meaningful contacts within their targets. However, apoptosis in other eye tissues is not a key event but rather a refinement. Thus, for the final development of the cornea, the control of keratocyte proliferation is more important than cell death events. The molecular mechanisms underlying apoptotic cell death have been conserved throughout evolution; however further investigations are needed to understand the key mechanisms of PCD in different tissues during development.
PY  - 2015
DO  - 10.1387/ijdb.150070ev
VL  - 59
IS  - 1-2-3
SP  - 63
EP  - 71
J2  - Int. J. Dev. Biol.
LA  - en
SN  - 0214-6282
SN  - 1696-3547
UR  - https://ijdb.ehu.eus/article/150070ev
Y2  - 2024/11/21/18:08:10
ER  -