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Abstract:
We compare vulva development between Caenorhaditis elegans and Pristionchus pacificus to study the evolution of developmental processes. Cell fate specification during vulva development differs in these two nematodes. In C. elegans, P8.p is a member of the vulva equivalence group and adopts a 3° fate under wild-type conditions. In contrast, several experiments indicate that P8.p in P. pacificus represents a novel cell type. First, P8.p is unable to respond to an inductive signal to form vulval tissue, but it can respond to lateral signal from the neighboring 1° cell P6.p. Second, P8.p provides a lateral inhibitory signal that prevents P5.p and P7.p, but not P6.p, from adopting a 1° fate. Third, P8.p provides a negative signal that inhibits gonad-independent vulva formation of P(5-7).p. To study P8.p specification, we screened for mutants with P8.p specification defects and identified three mutants in which P8.p behaves like a normal VPC. In one of these mutants, namely ped-17, the nucleus of P8.p has an abnormal size. Cell ablation experiments in ped-17 revealed that P8.p is able to respond to inductive signal from the gonad to form vulval tissue. Also, P8.p in this mutant cannot provide the lateral inhibitory signal. After P6.p ablation in these animals, either P5.p or P7.p can adopt a 1° fate. In addition, P8.p loses the function of providing negative signal in ped-17 mutant animals since gonad- independent vulva formation occurs. In another mutant, ped-7, P7.p migrates towards P8.p and forms an ectopic invagination. Genetic analysis revealed that ped-7 represents a multivulva mutation. We have mapped both mutants to the genetic linkage map of P. pacificus. ped-7 maps to chromosome V and is located between the markers S130 and S13. ped-17 is on chromosome II and is located between S111 and S24. Positional cloning of ped-7 and ped-17 is currently ongoing.
