Complex traits, including common disease-related traits, are affected by many different genes that function in multiple pathways and networks. The apoptosis, MAPK, Notch and Wnt signalling pathways play important roles in development and disease progression. At the moment we have a poor understanding of how allelic variation affects gene expression in these pathways at the level of translation. Here we report the effect of natural genetic variation on transcript and protein abundance involved in developmental signalling pathways in Caenorhabditis elegans. We used selected reaction monitoring to analyse proteins from the abovementioned four pathways in a set of recombinant inbred lines (RILs) generated from the wild-type strains Bristol N2 and Hawaii CB4856 to enable quantitative trait loci (QTL) mapping. Variation in gene expression was greater in the RILs than in the parental lines, at the proteome as well as at the transcriptome levels. We detected a trans-QTL on the left arm of chromosome II that affected protein abundance of the phosphatidylserine receptor protein PSR-1, and two separate QTLs that influenced embryonic and ionizing radiation-induced apoptosis on chromosome IV. Our results demonstrate that natural variation in C. elegans is sufficient to cause significant changes in signalling pathways both at the gene expression (transcript and protein abundance) and phenotypic levels.
Illumina HiSeq 2000 paired end sequencing; Illumina sequencing of C. elegans dauer entry daf-2(el370) sample 1-1 DauerEntryDAF2-1-1 polyA+ 101bp PE RNAseq random fragment library RW0001
Illumina HiSeq 2000 paired end sequencing; Illumina sequencing of C. elegans dauer entry daf-2(el370) sample 1-1 DauerEntryDAF2-1-1 polyA+ 100bp SE RNAseq random fragment library RW0001
Illumina HiSeq 2000 paired end sequencing; Illumina sequencing of C. elegans dauer entry daf-2(el370) sample 1-1 DauerEntryDAF2-1-1 polyA+ 100bp PE RNAseq random fragment library RW0001
Illumina HiSeq 2000 paired end sequencing; Illumina sequencing of C. elegans dauer entry daf-2(el370) sample 1-1 DauerEntryDAF2-1-1 polyA+ 101bp SE RNAseq random fragment library RW0001
We showed that KLF-1 is needed for longevity of isp-1(qm150);ctb-1(qm189) mutant specifically in adulthood. We aimed to determine the expression changes that occur specifically upon adulthood klf-1 RNAi compared to developmental RNAi that did not affect the lifespan of isp-1(qm150);ctb-1(qm189) mutant.