Data from: Loss-of-function mutations in the fruit softening gene POLYGALACTURONASE1 doubled fruit firmness in strawberry

Wildtype fruit of cultivated strawberry (Fragaria x ananassa) are
typically soft and highly perishable when fully ripe.  The
development of firm-fruited cultivars by phenotypic selection has greatly
increased shelf life, decreased post-harvest perishability, and driven the
expansion of strawberry production worldwide.  Hypotheses for the
firm-fruited phenotype include mutations affecting the expression of genes
encoding polygalacturonases that soften fruit by degrading cell wall
pectins.  Here we show that loss-of-function mutations in the
fruit softening gene POLYGALACTURONASE1 (PG1-6A1) double fruit firmness in
strawberry.  PG1-6A1 was one of three tandemly duplicated
polygalacturonase genes found to be in linkage disequilibrium with a
quantitative trait locus affecting fruit firmness on chromosome 6A.
PG1-6A1 was strongly expressed in soft-fruited (wildtype) homozygotes and
weakly expressed in firm-fruited (mutant) homozygotes.
 Genome-wide association, quantitative trait transcript, DNA
sequence, and expression-QTL analyses identified genetic variants in
linkage disequilibrium with PG1-6A1 that were positively correlated with
fruit firmness and negatively correlated with PG1-6A1 expression.
 An Enhancer/Suppressor-mutator (En/Spm) transposable element
insertion was discovered upstream of PG1-6A1 in mutant homozygotes that we
hypothesize transcriptionally downegulates the expression of PG1-6A1.
 The PG1-6A1 locus was incompletely dominant and explained 26-76%
of the genetic variance for fruit firmness among phenotypically diverse
individuals.  Additional loci are hypothesized to underlie the
missing heritability.  Highly accurate, codominant genotyping
assays were developed for modifying fruit firmness by marker-assisted
selection of the En/Spm insertion and SNPs associated with the PG1-6A1
locus.