Of the eight mutants that grew to bear fruit, fruits of six lines
exhibited lower accumulation of red pigmentation but two lines
produced full-ripening fruits (Fig. 3A). The full-ripening phenotype
was linked to the accumulation of RIN protein in the fruits, confirming
the importance of RIN for completing ripening. G2#13,
which bore light-orange fruits, abundantly accumulated a truncated
RIN protein. The truncated protein putatively lacks the Cterminal
44 amino acid residues (Fig. 3B and Supp. Table 2). We
previously proved that the C-terminal 27 amino acid residues of the
RIN protein are required to confer transcription activating activity
[26]. Thus, due to the defect in the activation domain, the truncated
protein of G2#13A has probably lost the activity to induce ripening.
The fruits of the RIN protein-defective T0 plants showed incomplete
ripening phenotype, but these plants might consist of chimera cells
or heterologous genotypes and thus the detailed mutation effects
should be evaluated in T1 or subsequent generations that harbor
mutations homozygously.