R J Sommer1, P W Sternberg. 1. Howard Hughes Medical Institute, California Institute of Technology, Pasadena 91125, USA.
Abstract
BACKGROUND: To understand how alterations in the molecular mechanisms underlying developmental processes generate a diversity of biological forms, comparative developmental biology can be combined with genetic analysis. The formation of the nematode vulva is one tractable system for such evolutionary developmental analysis, as much is understood about its development in Caenorhabditis elegans. In Caenorhabditis, six of twelve ventral epidermal cells form the 'vulva equivalence group'; although all six cells are competent to adopt vulval cell fates in response to an inductive signal, only three of these cells are induced to form vulval tissue. RESULTS: In some species of the nematode families Rhabditidae, Neodiplogastridae and Panagrolaimidae, the number of cells in the vulva equivalence group is limited by apoptosis and decreased responsiveness to inductive signals (competence). We have initiated a genetic analysis in one of these species, Pristionchus pacificus, to understand the evolution of the specification of ventral epidermal cells that are competent to generate the vulva. A ped-4 mutation restores competence to an incompetent cell. Mutation of either of two other genes of Pristionchus cause two anterior cells that die in wild-type to survive. A ped-5 mutation causes these cells to be competent to respond to inductive signals, expanding the equivalence group. A ped-6 mutation causes these cells to form ectopic, anterior vulva-like invaginations. CONCLUSIONS: During nematode evolution, apoptosis and change of competence alter the number and potency of ventral epidermal cells. The phenotypes of Pristionchus mutants suggest that alterations in homeotic gene control of anteroposterior patterning is involved in creating this cellular diversity.
BACKGROUND: To understand how alterations in the molecular mechanisms underlying developmental processes generate a diversity of biological forms, comparative developmental biology can be combined with genetic analysis. The formation of the nematode vulva is one tractable system for such evolutionary developmental analysis, as much is understood about its development in Caenorhabditis elegans. In Caenorhabditis, six of twelve ventral epidermal cells form the 'vulva equivalence group'; although all six cells are competent to adopt vulval cell fates in response to an inductive signal, only three of these cells are induced to form vulval tissue. RESULTS: In some species of the nematode families Rhabditidae, Neodiplogastridae and Panagrolaimidae, the number of cells in the vulva equivalence group is limited by apoptosis and decreased responsiveness to inductive signals (competence). We have initiated a genetic analysis in one of these species, Pristionchus pacificus, to understand the evolution of the specification of ventral epidermal cells that are competent to generate the vulva. A ped-4 mutation restores competence to an incompetent cell. Mutation of either of two other genes of Pristionchus cause two anterior cells that die in wild-type to survive. A ped-5 mutation causes these cells to be competent to respond to inductive signals, expanding the equivalence group. A ped-6 mutation causes these cells to form ectopic, anterior vulva-like invaginations. CONCLUSIONS: During nematode evolution, apoptosis and change of competence alter the number and potency of ventral epidermal cells. The phenotypes of Pristionchus mutants suggest that alterations in homeotic gene control of anteroposterior patterning is involved in creating this cellular diversity.