Genetic basis of plasticity of the growth- and flowering-related
phenotypes to N availability
Next, using genome-wide association (GWA) analysis, we investigated the
genetic architecture of plasticity of the four studied phenotypes in
response to N. To this end, we performed the GWA using the CV over all
three N conditions and, in addition, with the fold changes (FC) of the
phenotypic means between the optimal and limiting N conditions. GWA
analysis for the CVs of the four phenotypes identified only one
significant biallelic association for FT at the end of chromosome 1
(p-value = 1.41x10-7; Tables 1 and S4, Methods).
Interestingly, the GWA with the FC identified four SNPs on the same
locus on chromosome 1 that was associated with the CV of FT (Tables 1
and S4). We found no significant association for the other traits.
The low power of our dataset in detecting significant associations could
be due to the low heritability (i.e. low proportion of genotype x
environment variance from the total phenotypic variance) of the scored
plasticities (Sasaki et al., 2015; Tam et al., 2019). Another
explanation is that the low number of accessions that we used for our
study did not suffice to identify the loci with small effects. A third
explanation for the missing associations could be the incomplete set of
SNPs, since the initial GWA was performed with 250,000 SNPs (Horton et
al., 2012). To investigate if the lack of SNPs was the reason for the
few detected associations, we took advantage of those accessions with
fully sequenced genome, including 58 for ERD, 49 for FRD, 54 for FT and
44 for YIE, and performed GWA for the two plasticity scores. We detected
a significant association for the ERD on chromosome 1 to two biallelic
SNPs (Figure 3a; Tables 1 and S4).
Finally, we asked if the plasticity (scored as CV or FC) of the
phenotypes is controlled by the same genes that control the differences
in the mean trait values in the accessions. To investigate this
question, we performed the GWA with the mean value of the traits in the
three N conditions. We found a single significant association for ERD at
intermediate N on chromosome 1, but to a different SNP than that found
for the plasticity of ERD (Methods, Table S1). This implies that the
plasticity of the traits in response to N has a different genetic basis
than the one controlling the mean trait value in a single condition.