Post date: Dec 15, 2014 8:26:3 PM
We were able to map stripe to LG 8 in the A (and probably C) treatment. I now want to try with both combined (which is more relevant). This is part of a potential plan for this project (summarized at the end of this post).
I wrote a script to combine the data from both treatments (only MAF 5% in both), which is called: projects/timema_wgexperiment/gemma/scripts/combineTreatments.pl. This script produces two outfiles maf0.05geno_timemaCombined.txt and maf0.05LocListComb.txt, which include 3,743,817 SNPs. The data for A are first then C. I use cat to combine the phenotypes into pheno_stripeSamplesComb.txt (same order, A, then C).
I used the BVSR model in piMASS to examine the genetic basis of stripe variation in the combined data set. I ran 100 chains each with 3 million burn-in, 8 million additional steps, and a thinning interval of 5000. Here is an example below.
cd /local/scratch/
mkdir maf05strtimemaComb99
cd maf05strtimemaComb99
sleep 495
pimass-lin -g /home/A01963476/projects/timema_wgexperiment/gemma/maf0.05geno_timemaComb.txt -p /home/A01963476/projects/timema_wgexperiment/gemma/pheno_stripesamplesComb.txt -w 3000000 -s 8000000 -num 5000 -o pimass_timemaCombrep99 -cc
cd ..
rsync -avz maf05strtimemaComb99 /home/A01963476/projects/timema_wgexperiment/gemma/output_pimassMaf5str/
***** here are the plans for the project *****
1. PVE and no. SNPs estimates from piMASS (i.e. we show that there is likely some genetic variation for survival in the wild, but that genomic data explain only a minor proportion of the total varition in survival).
2. Compare model-averaged effects between the two treatments (C vs. A) to look for evidence of antagonstic pleiotropy (vs. conditional neutrality and variants that increase survival on both hosts). This would be very similar to what I have in the current paper on performance in L. melissa, but would involve whole genome data and survival in the wild (rather than in the lab).
3. Re-mapping of stripe (both treatments combined). We can then ask whether the stripe SNP(s) have elevated model-averaged effects in the survival analysis, and more importantly, whether the sign of the effects differ in the two treatments (i.e. stripe should be positively associated with survival in one treatment but not the other, right). We could thus show that even if antagonstic pleiotropy is not the rule, it holds for at least one or a few important loci (traits).
4. We could then ask whether the strip SNPs (and any other SNPs with evidence solid evidence of antagonistic pleiotropy for survival on the different host treatments) are structure by host plant in the natural populations (and perhaps even whether the extent that this is true varies as a function of gene flow).