Allelic-sensitivity vs gene-regulatory model
Sixty-three plasticity QTLs were identified among which 22 (35%) were
also identified when using the genotypic means; and 41 (65%) were
specific to plasticity. Via et al. (1995) proposed two genetic models –
the allelic-sensitivity and gene-regulatory models – among the
mechanisms involved in the genetic control of phenotypic plasticity.
These two models are distinguishable through QTL analysis (Ungerer et
al., 2003) with the expectation that allelic-sensitivity model will lead
to co-localization of genotypic means and plasticity QTLs, while a
distinct location of QTLs affecting mean and plasticity will likely
correspond to the gene-regulatory model (Kusmec et al., 2017). Regarding
our results, both models are suspected to regulate tomato plasticity,
even though the gene-regulatory model is predominant with 65% of the
plasticity QTLs that did not co-localize with genotypic means QTLs for
the same trait. In maize, using a larger number of environments and
traits, Kusmec et al. (2017) found similar results and even a higher
rate of distinct locations of plasticity and mean QTLs. Studying
plasticity as a trait per se is therefore of a major interest
since breeding in both direction (considering the mean phenotype and its
plasticity) is achievable. Through transcriptomic analyses, Albert et
al. (2018) observed that genotype x water deficit interaction was mostly
associated to trans- acting genes which could be assimilated to
the gene-regulatory model in agreement with our results.
Although the distinct location of QTLs detected on plasticity and
genotypic means could be confidently assigned to the action of genes in
interaction, their co-localization is not necessarily a case of
allelic-sensitivity regulation, especially if the QTL is in a large
region. Indeed, the allelic-sensitivity model assumes that a
constitutive gene is directly sensitive to the environment regulating
its expression across different environmental conditions, inducing hence
phenotypic plasticity. This is a very strong hypothesis regarding the
QTLs since the overlapping region between genotypic means and plasticity
could carry different causal variants in strong linkage disequilibrium
affecting either mean phenotype or plasticity. Thus, co-locating mean
and plasticity QTLs should be not automatically imputed to the
allelic-sensitivity model. We found a total of 22 constitutive QTLs
between genotypic means and plasticity for all 10 measured traits
(Supplemental Table 4). Considering the estimated QTL effects, the
variation patterns of the eight parental allelic classes were compared
between mean and PP QTL of the same trait. Only ten QTL showed
consistent allelic effects (Spearman correlation significant at 0.05
threshold level) strengthening the hypothesis of the allelic-sensitivity
model for these QTLs (Figure 6). Further studies should help to
elucidate and validate the candidate plasticity genes and to clarify
their functional mechanism.