The gene ced-9 of the nematode Caenorhabditis elegansacts to protect cells from programmed cell death. A mutation that abnormally activatesced-9 prevents the cell deaths that occur during normal C. elegans development. Conversely, mutations that inactivate ced-9 cause cells that normally live to undergo programmed cell death; these mutations result in embryonic lethality, indicating that ced-9 function is essential for development. The ced-9 gene functions by negatively regulating the activities of other genes that are required for the process of programmed cell death.

Caenorhabditis elegans gene ced-9 protects cells from programmed cell death

▪ Abstract For 600 million years, the two best-understood metazoan species, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster, have developed independent strategies for solving a biological problem faced by essentially all metazoans: how to generate two sexes in the proper proportions. The genetic program for sexual dimorphism has been a major focus of research in these two organisms almost from the moment they were chosen for study, and it may now be the best-understood general aspect of their development. In this review, we compare and contrast the strategies used for sex determination (including dosage compensation) between “the fly” and “the worm” and the way this understanding has come about. Although no overlap has been found among the molecules used by flies and worms to achieve sex determination, striking similarities have been found in the genetic strategies used by these two species to differentiate their sexes.

/pdf/vive-la-difference-males-vs-females-in-flies-vs-worms-4mr0ztu34y.pdf

VIVE LA DIFFÉRENCE:Males vs Females in Flies vs Worms

After programmed cell death, a cell corpse is engulfed and quickly degraded by a neighboring cell. For degradation to occur, engulfing cells must recognize, phagocytose and digest the corpses of dying cells. Previously, three genes were known to be involved in eliminating cell corpses in the nematode Caenorhabditis elegans: ced-1, ced-2 and nuc-1. We have identified five new genes that play a role in this process: ced-5, ced-6, ced-7, ced-8 and ced-10. Electron microscopic studies reveal that mutations in each of these genes prevent engulfment, indicating that these genes are needed either for the recognition of corpses by other cells or for the initiation of phagocytosis. Based upon our study of double mutants, these genes can be divided into two sets. Animals with mutations in only one of these sets of genes have relatively few unengulfed cell corpses. By contrast, animals with mutations in both sets of genes have many unengulfed corpses. These observations suggest that these two sets of genes are involved in distinct and partially redundant processes that act in the engulfment of cell corpses.

https://www.genetics.org/content/genetics/129/1/79.full.pdf

Genes required for the engulfment of cell corpses during programmed cell death in Caenorhabditis elegans.

The nematode Caenorhabditis elegans was chosen as a model genetic organism because its attributes, chiefly its hermaphroditic lifestyle and rapid generation time, make it suitable for the isolation and characterization of genetic mutants. The most important challenge for the geneticist is to design a genetic screen that will identify mutations that specifically disrupt the biological process of interest. Since 1974, when Sydney Brenner published his pioneering genetic screen, researchers have developed increasingly powerful methods for identifying genes and genetic pathways in C. elegans.

/pdf/the-art-and-design-of-genetic-screens-caenorhabditis-elegans-7criw8mhy0.pdf

The art and design of genetic screens: Caenorhabditis elegans

Most organisms reproduce through outcrossing, even though it comes with substantial costs. The Red Queen hypothesis proposes that selection from coevolving pathogens facilitates the persistence of outcrossing despite these costs. We used experimental coevolution to test the Red Queen hypothesis and found that coevolution with a bacterial pathogen (Serratia marcescens) resulted in significantly more outcrossing in mixed mating experimental populations of the nematode Caenorhabditis elegans. Furthermore, we found that coevolution with the pathogen rapidly drove obligately selfing populations to extinction, whereas outcrossing populations persisted through reciprocal coevolution. Thus, consistent with the Red Queen hypothesis, coevolving pathogens can select for biparental sex.

/pdf/running-with-the-red-queen-host-parasite-coevolution-selects-2m54zvz4fz.pdf

Leilani M. Miller

Papers

xol-1: A gene that controls the male modes of both sex determination and X chromosome dosage compensation in C. elegans