Segregation of homologous chromosomes during meiosis depends on linkages (chiasmata) created by crossovers and on selective release of a subset of sister chromatid cohesion at anaphase I. DuringCaenorhabditis elegans meiosis, each chromosome pair forms a single crossover, and the position of this event determines which chromosomal regions will undergo cohesion release at anaphase I. Here we provide insight into the basis of this coupling by uncovering a large-scale regional change in chromosome axis composition that is triggered by crossovers. We show that axial element components HTP-1 and HTP-2 are removed during late pachytene, in a crossover-dependent manner, from the regions that will later be targeted for anaphase I cohesion release. We demonstrate correspondence in position and number between chiasmata and HTP-1/2-depleted regions and provide evidence that HTP-1/2 depletion boundaries mark crossover sites. In htp-1 mutants, diakinesis bivalents lack normal asymmetrical features, and sister chromatid cohesion is prematurely lost during the meiotic divisions. We conclude that HTP-1 is central to the mechanism linking crossovers with late-prophase bivalent differentiation and defines the domains where cohesion will be protected until meiosis II. Further, we discuss parallels between the pattern of HTP-1/2 removal in response to crossovers and the phenomenon of crossover interference.[Keywords: Meiosis; chromosome axes; crossover; sister chromatid cohesion; chromosome remodeling; crossover interference] Supplemental material is available at http://www.genesdev.org. Received May 12, 2008; revised version accepted August 18, 2008. In sexually reproducing organisms, diploid germ cells produce haploid gametes through the specialized cell division program of meiosis. At the onset of meiosis, DNA is replicated and sister chromatid cohesion (SCC) is established (Nasmyth and Schleiffer 2004). In contrast to mitotic cell cycles, this single round of meiotic DNA replication is followed by two rounds of cell division, the first segregating homologous chromosomes (homologs), and the second segregating sister chromatids (Petronczki et al. 2003). This pattern of segregation requires an extended prophase during which chromosomes must assemble meiosis-specific axial structures, locate, and align with their homologs, stabilize this alignment through assembly of the synaptonemal complex (SC), and undergo crossover recombination events between their DNA molecules (Page and Hawley 2003). Crossovers that form in this context play a crucial role in promoting meiotic chromosome segregation, as they collaborate with SCC (on domains flanking the crossover site) to form the basis of chiasmata, cytologically visible connections between the homologs that are revealed upon SC disassembly and structural remodeling of chromosomes during late prophase (Jones 1987). Chiasmata allow homologs to remain connected while orienting away from each other toward opposite poles of the metaphase I spindle. Subsequently, the SCC that maintains the co...

Behavioural innovation and morphological adaptation are intrinsically linked but their relationship is often poorly understood. In nematodes, a huge diversity of feeding morphologies and behaviours can be observed to meet their distinctive dietary and environmental demands. Pristionchus and their relatives show varied feeding activities, both consuming bacteria and also predating other nematodes. In addition, Pristionchus nematodes display dimorphic mouth structures triggered by an irreversible developmental switch, which generates a narrower mouthed form with a single tooth and a wider mouthed form with an additional tooth. However, little is known about the specific predatory adaptations of these mouth forms or the associated mechanisms and behaviours. Through a mechanistic analysis of predation behaviours, in particular in the model organism Pristionchus pacificus, we reveal multifaceted feeding modes characterised by dynamic rhythmic switching and tooth stimulation. This complex feeding mode switch is regulated by the neurotransmitter serotonin in a previously uncharacterised role, a process that appears conserved across several predatory nematode species. Furthermore, we investigated the effects of starvation, prey size and prey preference on P. pacificus predatory feeding kinetics, revealing predation to be a fundamental component of the P. pacificus feeding repertoire, thus providing an additional rich source of nutrition in addition to bacteria. Finally, we found that mouth form morphology also has a striking impact on predation, suppressing predatory behaviour in the narrow mouthed form. Our results therefore hint at the regulatory networks involved in controlling predatory feeding and underscore P. pacificus as a model for understanding the evolution of complex behaviours.

Environment shapes development through a phenomenon called developmental plasticity. Deciphering its genetic basis has potential to shed light on the origin of novel traits and adaptation to environmental change. However, molecular studies are scarce, and little is known about molecular mechanisms associated with plasticity. We investigated the gene regulatory network controlling predatory vs. non-predatory dimorphism in the nematode Pristionchus pacificus and found that it consists of genes of extremely different age classes. We isolated mutants in the conserved nuclear hormone receptor nhr-1 with previously unseen phenotypic effects. They disrupt mouth-form determination and result in animals combining features of both wild-type morphs. In contrast, mutants in another conserved nuclear hormone receptor nhr-40 display altered morph ratios, but no intermediate morphology. Despite divergent modes of control, NHR-1 and NHR-40 share transcriptional targets, which encode extracellular proteins that have no orthologs in Caenorhabditis elegans and result from lineage-specific expansions. An array of transcriptional reporters revealed co-expression of all tested targets in the same pharyngeal gland cell. Major morphological changes in this gland cell accompanied the evolution of teeth and predation, linking rapid gene turnover with morphological innovations. Thus, the origin of feeding plasticity involved novelty at the level of genes, cells and behavior. Author summaryRather than following a pre-determined genetic "blueprint", organisms can adjust their development when they perceive relevant environmental signals-a phenomenon called plasticity. This improves performance in changing environment and may also affect how species evolve. To learn how plasticity works on the mechanistic genetic level, we investigated the roundworm Pristionchus pacificus. It may develop either as a toothed predator or as a narrow-mouthed microbe-eater depending on food source and population density, an ability that evolved less than 100 million years ago. Previous studies identified switch PLOS GENETICS PLOS Genetics | https://doi.

Self-recognition is observed abundantly throughout the natural world, regulating diverse biological processes. Although ubiquitous, often little is known of the associated molecular machinery, and so far, organismal self-recognition has never been described in nematodes. We investigated the predatory nematode Pristionchus pacificus and, through interactions with its prey, revealed a self-recognition mechanism acting on the nematode surface, capable of distinguishing self-progeny from closely related strains. We identified the small peptide SELF-1, which is composed of an invariant domain and a hypervariable C terminus, as a key component of self-recognition. Modifications to the hypervariable region, including single–amino acid substitutions, are sufficient to eliminate self-recognition. Thus, the P. pacificus self-recognition system enables this nematode to avoid cannibalism while promoting the killing of competing nematodes.

The microaerophilic bacterium Campylobacter jejuni is a significant food-borne pathogen and is predicted to possess two terminal respiratory oxidases with unknown properties. Inspection of the genome reveals an operon (cydAB) apparently encoding a cytochrome bd-like oxidase homologous to oxidases in Escherichia coli and Azotobacter vinelandii. However, C. jejuni cells lacked all spectral signals characteristic of the high-spin hemes b and d of these oxidases. Mutation of the cydAB operon of C. jejuni did not have a significant effect on growth, but the mutation reduced formate respiration and the viability of cells cultured in 5% oxygen. Since cyanide resistance of respiration was diminished in the mutant, we propose that C. jejuni CydAB be renamed CioAB (cyanide-insensitive oxidase), as in Pseudomonas aeruginosa. We measured the oxygen affinity of each oxidase, using a highly sensitive assay that exploits globin deoxygenation during respiration-catalyzed oxygen uptake. The CioAB-type oxidase exhibited a relatively low affinity for oxygen (K m ‫؍‬ 0.8 M) and a V max of >20 nmol/mg/s. Expression of cioAB was elevated fivefold in cells grown at higher rates of oxygen provision. The alternative, ccoNOQP-encoded cyanide-sensitive oxidase, expected to encode a cytochrome cb-type enzyme, plays a major role in the microaerobic respiration of C. jejuni, since it appeared to be essential for viability and exhibited a much higher oxygen affinity, with a K m value of 40 nM and a V max of 6 to 9 nmol/mg/s. Lowtemperature photodissociation spectrophotometry revealed that neither oxidase has ligand-binding activity typical of the heme-copper oxidase family. These data are consistent with cytochrome oxidation during photolysis at low temperatures.