Gilberto Bento et al. (2008) European Worm Meeting "Genetic and environmental control of phenotypic plasticity in the mouth forms of Pristionchus pacificus"

Gilberto Bento, Ralf J Sommer, Akira Ogawa

[European Worm Meeting, 2008]

Nematodes of the genus Pristionchus show a mouth dimorphism that underlies. different feeding ecologies. Eurystomatous worms have denticles and can. feed on bacteria, fungi and nematodes, whereas stenostomatous worms have no. denticles and only feed on bacteria. Using selection inbred lines of. Pristionchus pacificus, we have shown that this is a case of. environmentally induced phenotypic plasticity and that there is genetic. variation between different strains for the switch mechanism. We have. proceeded to investigate both the environmenal and the genetic basis of. this phenomenon. A strong response to starvation and/or high population. density in early larval development was observed in all analyzed strains,. with a dramatic increase in the percentage of eurystomatous worms.. Interestingly, this is not observed in daf-d (dauer formation defective). mutants. Furthermore, we have also observed that i) the presence of P.. pacificus dauer pheromone influences the mouth form switch mechanism, ii). worms that go through the dauer stage are invariably stenostomatous worms,. and iii) a positive correlation between percentage of eurystomatous worms. and dauer induction index among natural strains. All together, these. results suggest a link between the genetic control of dauer formation and. mouth form regulation, which are both responsive to similar environmental. triggers. In order to investigate which loci are contributing for the mouth. form phenotypic plasticity, we use i) a library of Recombinant Inbred Lines. (RILs) and ii) analysis of dauer-defective mutants. We have so far. identified two genes involved in mouth form regulation. Currently, we are. genotyping the RILs for QTL analysis and also mapping the daf-d mutants. that show a mouth form phenotype.. Do not add objects such as pictures, boxes, headers, footers, footnotes,. etc.

Akira Ogawa et al. (2010) East Asia Worm Meeting "Ppa-daf-16 regulates Dauer Formation but not Buccal Cavity Dimorphism in Pristionchus pacificus"

Gabi Bartelmes, Gilberto Bento, Akira Ogawa, Christoph Dieterich, Ralf J. Sommer

[East Asia Worm Meeting, 2010]

Based on knowledge obtained from C. elegans, we are exploring how the regulatory mechanisms for dauer formation evolved, using the genetically tractable nematode Pristionchus pacificus and other nematode species. So far we and others have shown that the nuclear hormone receptor DAF-12 and its ligands represent an evolutionarily conserved mechanism for dauer formation in free-living species as well as infective larva formation in parasitic species [1, 2]. In addition to the developmental plasticity of dauer formation, P. pacificus shows plasticity in buccal cavity (BC) formation in the adult stage. One morph called eurystomatous has a wide and shallow mouth opening and is specialized for predation and fungi-feeding whereas the other morph, stenostomatous, has a narrow and deep mouth opening and is specialized for bacteria-feeding. This dimorphism is regulated by at least two environmental factors including starvation and dauer pheromone [3]. In addition multiple daf-d mutants that include daf-12 strains also show defects in the regulation of BC dimorphism, suggesting that the mechanisms for dauer formation and BC dimorphism are largely overlapping. However, we have found several other strains that show strong daf-d phenotype but normal regulation of BC dimorphism. To identify the gene responsible for these mutations, we sequenced the genome of the mutant strains using Illumina Genome Analyzer and identified mutations in the orthologue of daf-16. Our results suggest that daf-16 represents one of the evolutionarily conserved mechanisms for dauer formation and among the two regulatory mechanisms that involve DAF-12 and DAF-16, only DAF-12 steroid signaling was co-opted for the regulation of BC dimorphism. We are currently investigating how upstream regulators of these two transcription factors evolved. Reference 1. Ogawa et al. (2009). Curr Biol 19, 67-71. 2. Wang et al. (2009). PNAS 106, 9138-9143. 3. Bento et al. Nature in press.

Ray Hong et al. (2008) Development & Evolution Meeting "Whole-Genome Sequencing and Analyses of a Pristionchus pacificus "Doppleganger" Strain with Divergent Phenotypes"

Hanh Witte, Simone Kienle, Detlef Weigel, Korbinian Schneeberger, Ralf Sommer, Gilberto Bento, Stephan Ossowski, Christoph Dieterich, Christa Lanz, Ray Hong

[Development & Evolution Meeting, 2008]

Recently diverged wild populations with low genetic differences coupled with strikingly distinct phenotypes offer rare opportunities to thoroughly characterize the genotype-to-phenotype relationships of natural variants. We used the massively parallel sequencing platform, the Solexa Sequence Analyzer (Illumina Inc.), to sequence the entire 169 MB genome of Pristionchus pacificus Poland RS106, a closely related strain to the reference strain California PS312. We identified between 700-6200 candidate SNPs/indels and so far validated 105 of these by traditional Sanger sequencing of PCR products from both strains. The resulting estimated true SNP frequency may be up to 10,000x less than the number of polymorphisms in the P. pacificus mapping strain Washington PS1843 (~1:26) as well as ~160x less frequent than between the C. elegans N2 and CB4858 strains (~1:1500) found in a similar Solexa study(1). Nevertheless, this estimate confirmed our expected low SNP count based on previous Sanger sequencing of randomly chosen ~30 kb genomic regions of the Poland strain. In order to map the loci responsible for the phenotypic variations in mouth dimorphism, vulva induction, egg laying, and chemoattraction to insect pheromones, we genotyped ~1000 Recombinant Inbred Lines from California/Poland crosses using ~100 confirmed SNPs distributed on all six chromosomes. Preliminary findings for loci linked to differences in mouth dimorphisms and egg laying will be discussed. Thus, the combination of the Solexa platform and QTL mapping in genetically similar but phenotypically disparate novel strains offers a rapid, powerful way to compile a nearly complete list of SNPs associated with phenotypic differences among natural variants.

Susoy, Vladislav et al. (2014) Evolutionary Biology of Caenorhabditis and Other Nematodes "EVOLUTIONARY DIVERSIFICATION THROUGH THE GAIN AND LOSS OF DEVELOPMENTAL PLASTICITY"

Sommer, Ralf J., Susoy, Vladislav, Ragsdale, Erik J.

[Evolutionary Biology of Caenorhabditis and Other Nematodes, 2014]

Developmental plasticity is common among plants and animals, yet its role in mediating evolutionary processes is debated. Several species of Rhabditina, including Pristionchus pacificus, can execute two alternative mouth phenotypes, one of which is associated with predatory feeding. Studies in P. pacificus have revealed that environmental factors act through a conserved genetic pathway that enables a rapid developmental response to the environment (Bento et al., 2010). In addition, a developmental switch that controls the expression of the alternative mouth phenotypes was recently identified (Ragsdale et al., 2013). In contrast, little is known about the macroevolutionary potential of the mouth plasticity. We studied the relationship between plasticity and morphological change by a macroevolutionary analysis of nematode mouthparts when accompanied by a dimorphism. To test whether plasticity facilitates or hinders morphological change, we analyzed variation in form and complexity in 90 nematode species with or without a mouth dimorphism. Our analyses revealed a two-step process of morphological diversification associated with the gain and loss of plasticity. First, acquisition of a dimorphism was accompanied by an increase in complexity, including structural innovations such as moveable teeth. Second, the fixation of a single mouth-phenotype in several nematode lineages was associated with a decrease in mouth complexity but a sharp increase in evolutionary rates when measured as change of shape and size. Thus, plasticity facilitates phenotypic diversification by fostering evolutionary novelties, whereas subsequent loss of the dimorphism enables acceleration of evolution by releasing novel morphologies from developmental constraints. 1. G. Bento, A. Ogawa, R. J. Sommer. Nature 466, 494-497 (2010). 2. E. J. Ragsdale, M. R. Muller, C. Rodelsperger, R. J. Sommer, Cell 155, 922-933 (2013).