GROWTH, PROLIFERATION, AND CELL-DEATH IN THE ONTOGENY OF TRANSIENT DRG (FRORIEPS GANGLIA) OF CHICK-EMBRYOS

A striking example of axial patterning in nervous system development i s the unusual fate of dorsal root ganglia (DRG) that develop in the mo st rostral somites, the Froriep's ganglia. In amniotes, the DRG that d evelop adjacent to the occipital (cranial) and the first cervical segm ents of the CNS ''disappear'' early in embryonic development. In contr ast, all other DRG are present throughout the animal's life. We here r eexamine in greater detail the ontogeny of the longest surviving Frori ep's ganglion of the chick embryo, DRG C-2. By 50 h of development (st age, st. 15), an anlagen of a DRG had formed in C-2 that was indisting uishable from those of adjacent ''permanent'' ganglia. At st. 18 [embr yonic day (E)2.5+], the C-2 DRG had the same shape and volume as perma nent ganglia C-5 and C-6. C-2's development first diverged from that o f normal DRG at st. 19 (E3-), when C-2 was observed to be half the siz e and shaped differently from its neighbors, and its peripheral nerve root began to degenerate. Two cellular mechanisms appear to contribute to the reduced size of C-2 compared to normal DRG at st. 20 at this e arly stage: lower proliferation and higher apoptosis rates. One-third fetter C-2 cells were found to be in the S phase when compared to neig hboring ganglia, and apoptotic cells were more than three times more a bundant in C-2 than in conventional DRG at this stage. The C-2 DRG con tinued to grow, but at a slower pace than neighboring ganglia through st. 32 (E7). At the height of the normal programmed DRG cell death in normal cervical DRG at st. 28 (E6), even more massive apoptosis occurr ed in C-2, which resulted in the absence of this ganglion in 80% of st . 36 (E10) embryos. A recent study demonstrated that the overexpressio n of a single Hox gene can ''rescue'' the C-2 DRG in transgenic mice. We speculate that Hox genes may produce the difference in fate between C-2 and normal DRG by modulating proliferation and apoptosis via modi fied neurotrophic factor and/or receptor expression. (C) 1996 John Wil ey & Sons, Inc.