Ivo M Chelo et al. (2010) Evolutionary Biology of Caenorhabditis and Other Nematodes "RECOMBINATION LOAD IN C.ELEGANS EXPERIMENTAL POPULATIONS"

Henrique Teotonio, Ivo M Chelo, Sara Carvalho

[Evolutionary Biology of Caenorhabditis and Other Nematodes, 2010]

The interaction of recombination and natural selection in large populations is poorly understood at the empirical level. We have constructed populations of C. elegans that segregate large amounts of genetic variation and alternative mating systems. Upon these populations experimental evolution was performed, in well-defined laboratory conditions, for 100 generations, and patterns of DNA sequence diversity were characterized for two chromosomes at a density of approximately 100kb. We observe that there is extensive natural selection in single-marker frequencies which cannot be explained by initial gametic linkage disequilibrium. With standing genetic variation outcrossing rates have no differential effects on adaptation, unless effective recombination rates are explicitly sought by inbreeding of evolving outbred populations. When this is done we find that higher outcrossing leads to higher recombination that is responsible for the break-up of several high fitness polygenic polymorphisms during initial experimental evolution, while lower effective recombination appears to generate the same kind of balanced polymorphisms after 100 generations. These observations will be briefly discussed in the context of evolutionary theory.

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.

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.

Sarfarazhussain Farooqui et al. (2006) European Worm Meeting "A GFP Reporter Based Screen for the Notch Target Genes during Vulval Development"

Sarfarazhussain Farooqui, ALEX HAJNAL, Ivo Rimann

[European Worm Meeting, 2006]

Sarfarazhussain Farooqui, Ivo Rimann and Alex Hajnal. During hermaphrodite vulval development, lateral signaling from the primary vulval precursor cell (VPC) P6.p activates the LIN-12 Notch pathway in the neighbouring secondary VPCs P5.p and P7.p. The LIN-12 Notch signal inhibits primary fate specification and promotes the secondary vulval fate by activating transcription factors of the CSL family, which turn on the expression of specific target genes.. LIN-12 Notch targets usually contain clusters of CSL binding sites (RTGGGAA) in their promoter/enhancer regions. To identify new target genes of the LIN-12 Notch pathway in a systematic way, we searched the C. elegans genome sequence for genes containing clusters of three or more CSL sites within 2 kbp upstream of the start codon. We further refined our list of candidate Notch targets by taking into consideration only those genes in which the putative CSL sites are conserved in the C. briggsae orthologs. Promoter-GFP fusion constructs for the 23 strongest candidate genes were made by fusion PCR and injected into wild-type worms to create transgenic lines. Details on the expression patterns of the reporter constructs generated so far will be presented at the meeting.

Ivo Rimann et al. (2006) European Worm Meeting "The Transcription Factor EGL-43 is Necessary for Anchor Cell Invasion during Vulval Development"

Ivo Rimann, ALEX HAJNAL

[European Worm Meeting, 2006]

Ivo Rimann and Alex Hajnal. For proper egg-laying by the hermaphrodite, the uterus has to become firmly connected to the vulva during late larval development. The anchor cell (AC), a specialized cell in the somatic gonad, coordinates vulval and uterus development and initiates the formation of the connection between these two tissues.. During the L3 larval stage, the AC induces six neighboring ventral uterine (VU) cells to adopt the Pi cell fate. Around the same time of development, the basal laminas separating the uterus from the vulva begin to dissolve and the AC invades the vulval tissue by extending a process between the primary cells (Sherwood et al., 2003). In this way, the AC connects the vulval and uterine tissues.. In an RNAi-based screen for genes regulating vulval morphogenesis, we have found that knock-down of egl-43 causes a penetrant protruding vulva (Pvl) phenotype because the connection between the uterus and vulva is not formed correctly. egl-43 encodes a zinc finger transcription factor homologous to the human EVI1 proto-oncogene. Closer examination showed that in egl-43 RNAi animals the basal lamina under the AC is not removed, which prevents the AC from invading the vulval tissue. In addition, egl-43 RNAi animals show defects in the specification of the Pi cell fate. Similar defects in AC invasion have been reported for fos-1 mutants (Sherwood et al., 2005), and like fos-1, a transcriptional egl-43p::gfp reporter is expressed at high levels in the AC and at lower levels in the adjacent VU cells. Moreover, egl-43p::gfp expression in the AC is 5-fold reduced in a fos-1(0) background, indicating that FOS-1 promotes AC invasion at least in part by up-regulating egl-43 expression in the AC.