A 34K SNP genotyping array for Populus trichocarpa: design, application to the study of natural populations and transferability to other Populus species.

Genetic mapping of quantitative traits requires genotypic data for large numbers of markers in many individuals. For such studies, the use of large single nucleotide polymorphism (SNP) genotyping arrays still offers the most cost-effective solution. Herein we report on the design and performance of a SNP genotyping array for Populus trichocarpa (black cottonwood). This genotyping array was designed with SNPs pre-ascertained in 34 wild accessions covering most of the species latitudinal range. We adopted a candidate gene approach to the array design that resulted in the selection of 34 131 SNPs, the majority of which are located in, or within 2 kb of, 3543 candidate genes. A subset of the SNPs on the array (539) was selected based on patterns of variation among the SNP discovery accessions. We show that more than 95% of the loci produce high quality genotypes and that the genotyping error rate for these is likely below 2%. We demonstrate that even among small numbers of samples (n = 10) from local populations over 84% of loci are polymorphic. We also tested the applicability of the array to other species in the genus and found that the number of polymorphic loci decreases rapidly with genetic distance, with the largest numbers detected in other species in section Tacamahaca. Finally, we provide evidence for the utility of the array to address evolutionary questions such as intraspecific studies of genetic differentiation, species assignment and the detection of natural hybrids.

Chemosensory neurons function in parallel to mediate a pheromone response in C. elegans.

Formation of the C. elegans dauer larva is repressed by the chemosensory neurons ADF, ASI, and ASG. Mutant analysis has defined two parallel genetic pathways that control dauer formation. By killing neurons in these mutants, we show that mutations in one of these genetic pathways disrupt dauer repression by ADF, ASI, and ASG. One gene in this pathway is daf-7, which encodes a TGFbeta-related protein. We find that daf-7::GFP fusions are expressed specifically in ASI and that expression is regulated by dauer-inducing sensory stimuli. We also show that a different chemosensory neuron, ASJ, functions in parallel to these neurons to induce dauer formation. Mutations in the second genetic pathway activate dauer formation in an ASJ-dependent manner. Thus, the genetic redundancy in this process is reflected at the neuronal level.

Mutations affecting the chemosensory neurons of Caenorhabditis elegans.

We have identified and characterized 95 mutations that reduce or abolish dye filling of amphid and phasmid neurons and that have little effect on viability, fertility or movement. Twenty-seven mutations occurred spontaneously in strains with a high frequency of transposon insertion. Sixty-eight were isolated after treatment with EMS. All of the mutations result in defects in one or more chemosensory responses, such as chemotaxis to ammonium chloride or formation of dauer larvae under conditions of starvation and overcrowding. Seventy-five of the mutations are alleles of 12 previously defined genes, mutations which were previously shown to lead to defects in amphid ultrastructure. We have assigned 20 mutations to 13 new genes, called dyf-1 through dyf-13. We expect that the genes represented by dye-filing defective mutants are important for the differentiation of amphid and phasmid chemosensilla.