How species arise is one of the fundamental questions of biology and, ironically, one that stumped Darwin in his book On the Origin of Species, where he referred to speciation as the “mystery of mysteries.” Today, understanding speciation remains a grand challenge. The process of speciation involves the evolution of reproductive barriers between populations within a species so that a single species can split and become two. Thus, identifying the mechanisms of reproductive isolation is crucial to understanding how speciation occurs. There are many types of reproductive barriers that isolate existing species (e.g. ecological isolation, behavioral isolation), but the barriers that currently isolate species are not necessarily the same barriers that drove their speciation.

When closely related species are capable of interbreeding, they typically produce hybrid progeny that are inviable or sterile. That is, they are reproductively isolated by postzygotic mechanisms. According to the Bateson-Dobzhansky-Muller model, postzygotic reproductive isolation evolves by the accumulation of genetic incompatibilities between populations. It is thought that hybrid incompatibility arises due to gradual divergence in coevolving genes as populations adapt to distinct ecological niches. But what are the genes? Does every speciation event involve unique genes or are there “speciation genes” that are repeatedly used as the substrates of this evolutionary process? And how do these genes evolve to create reproductive barriers – does this occur by a neutral or adaptive mechanism?

Screen Shot 2015-12-01 at 1.54.02 PM

We have previously reported an interesting intraspecific hybrid incompatibility within the nematode C. elegans. This incompatibility is mediated by a novel selfish genetic element consisting of two adjacent genes encoding a sperm-expressed paternal effect toxin called PEEL-1 and its zygotic antidote ZEEL-1. In the absence of ZEEL-1, sperm-supplied PEEL-1 causes lethal defects at a late stage of embryogenesis (photos to the right.) Thus, these genes fit the pattern of hybrid incompatibility genes that are in genetic conflict with their host genome: the peel-1/zeel-1 element serves no apparent role other than to propagate itself by eliminating progeny that do not inherit the element. Although we have worked out the genetic mechanism of this incompatibility and identified the genes, we know little about the cellular mechanisms of toxin and antidote activity.

In a searching to find other hybrid incompatibilities, we have been looking for new species of Caenorhabditis. Extensive sampling of rotting fruits by our lab and others has led to the discovery of forty-two new species of Caenorhabditis as well as the isolation of hundreds of additional strains of many known species. At least two of the species pairs (C. briggsae/C. nigoni and C. remanei/C. latens) give rise to fertile hybrid progeny and are already being studied genetically by other laboratories. The large number of isolates of some species has also led to the discovery of intraspecific incompatibilities (like peel-1/zeel-1 in C. elegans) that can act as partial reproductive barriers. Thus, Caenorhabditis is an excellent system to determine genes that mediate hybrid incompatibility at different levels of reproductive isolation so that broader questions related to speciation can be asked.