Noble, Luke et al. (2017) International Worm Meeting "Polygenicity and epistasis underlie fitness-proximal traits in the Caenorhabditis elegans multiparental experimental evolution (CeMEE) panel."

Guzella, Thiago, Noble, Luke, Riccardi, David, Dayarian, Adel, Afonso, Bruno, Shraiman, Boris, Teotonio, Henrique, Rockman, Matthew, Pino-Querido, Ania, Crist, Anna, Chelo, Ivo, Ammerman, Patrick, Cavalho, Sara

[International Worm Meeting, 2017]

Understanding the genetic basis of complex traits remains a major challenge in biology. Polygenicity, phenotypic plasticity and epistasis contribute to phenotypic variance in ways that are rarely clear. This uncertainty is problematic for estimating heritability, for predicting individual phenotypes from genomic data, and for parameterizing models of phenotypic evolution. Here we report a recombinant inbred line (RIL) quantitative trait locus (QTL) mapping panel for the hermaphroditic nematode Caenorhabditis elegans, the C. elegans multiparental experimental evolution (CeMEE) panel. The CeMEE panel, comprising 507 RILs, was created by hybridization of 16 wild isolates, experimental evolution at moderate population sizes for 140-190 discrete generations, and inbreeding by selfing for 13-16 generations. The panel contains around 22% of single nucleotide polymorphisms known to segregate in natural populations, and complements existing mapping resources for C. elegans by providing high nucleotide diversity across >95% of the genome, and fine-scale mapping resolution. We apply it to study the genetic basis of two fitness components, fertility and adult hermaphrodite body size, with high broad sense heritability in the CeMEE. While simulations show we should detect common alleles with additive effects as small as 5%, at gene-level resolution, the genetic architectures of these traits does not feature such alleles. We instead find that a significant fraction of trait variance, particularly for fertility, can be explained by sign epistasis with weak main effects. Multiple interactions involving egl-18 (and potentially the functionally related flanking genes egl-4 and elt-6 as well) are highly influential for fertility, consistent with selection for embryo retention during experimental evolution. Phenotype prediction, while generally poor (r2<10%), requires modeling epistasis for optimal accuracy, with most variance attributed to the highly recombinant, rapidly evolving chromosome arms.

Noble, Luke et al. (2017) International Worm Meeting "The C. elegans multiparent experimental evolution mapping panel."

Dayarian, Adel, Cavalho, Sara, Guzella, Thiago, Riccardi, David, Ammerman, Patrick, Teotonio, Henrique, Pino-Querido, Ania, Rockman, Matthew, Shraiman, Boris, Crist, Anna, Afonso, Bruno, Noble, Luke, Chelo, Ivo

[International Worm Meeting, 2017]

We report a recombinant inbred line (RIL) quantitative trait locus (QTL) mapping panel for the hermaphroditic nematode Caenorhabditis elegans, the C. elegans multiparental experimental evolution (CeMEE) panel. The CeMEE panel, comprising 507 RILs, was created by hybridization of 16 wild isolates, experimental evolution at moderate population sizes for 140-190 discrete generations, and inbreeding by selfing for 13-16 generations. The panel contains around 22% of single nucleotide polymorphisms known to segregate in natural populations, and complements existing mapping resources for C. elegans by providing high nucleotide diversity across >95% of the genome, and fine-scale mapping resolution.

Sara Vassalli et al. (2006) European Worm Meeting "Identification of Genes required for Anchor Cell Attachment and Invasion during Vulval Development"

ALEX HAJNAL, Sara Vassalli

[European Worm Meeting, 2006]

Sara Vassalli and Alex Hajnal. During vulval development in the hermaphrodite, three out of six equivalent vulval precursor cells (the VPCs P3.p to P8.p) are induced by a signal from the gonadal anchor cell (AC). The LIN-3 EGF growth factor produced by the AC activates the EGFR/RAS/MAPK pathway in the VPCs to specify the primary cell fate. Prior to vulval induction, the gonad is separated from the VPCs by two basal laminas covering each tissue such that the position of the AC relative to the VPCs is variable when the animal moves. At the time of vulval induction in the early L3 stage, however, the AC attaches to the basal side of the future primary cell P6.p. After the first round of vulval cell divisions (Pn.px stage), the basal laminas separating the gonad from the vulval cells start to dissolve precisely under the AC. After the second round of divisions (Pn.pxx stage), the basal laminas between the AC and the four primary vulval cells are interrupted, and the AC invades the vulval tissue.. While the mechanism of vulval induction is well studied, less is known about genes regulating the attachment of the AC to P6.p and the following invasion step. To study these two processes, we performed a forward genetic screen for mutants with defects in AC positioning and/or invasion. Since worms with an abnormal or missing connection between the gonad and the vulva usually display a protruding vulva (Pvl) phenotype, we first screened for animals with a Pvl phenotype and then examined them for defects in the positioning or invasion of the AC. Among 5300 F1 clones, we identified 8 sterile mutants with a misplaced AC and 2 mutants, in which the AC is normally positioned but fails to dissolve the basal laminas and invade the vulval tissue. Details about the cloning and analysis of the genes identified in this screen will be presented at the meeting.