| Description |
Fruit softening is associated with the degradation of cell wall components such as pectin, cellulose, and hemicellulose. Despite extensive research on pectin and its associated enzymes, little is known about the role of cellulose in fruit softening. Here, we highlight the pivotal role of two transcription factors SlERF.H5 and SlERF.H7 in promoting cell wall formation and fruit firmness. Knockout of SlERF.H5 or SlERF.H7 or both genes led to reduced cell wall thickness with promoted locule liquefaction and lower cellulose content from early fruit developmental stages. Conversely, overexpression of these genes resulted in thicker cell walls with higher levels of cellulose. We further demonstrated that SlERF.H5 and SlERF.H7 function as transcriptional activators on the expression of cellulose synthesis gene SlCESA3. In addition, we found that overexpression of SlERF.H5 or SlERF.H7 resulted in dramatic dwarf plants with decreased GA levels. SlERF.H5 and SlERF.H7 inhibited GA synthesis by repressing the expression of key GA biosynthesis genes GA20ox1. Moreover, a newly identified LPL-motif at the C-terminal of SlERF.H5 and SlERF.H7 determined their bifunction in transcriptional activation and repression. Overall, our findings demonstrated a dual role of two ERF transcription factors by activating or repressing different target genes dependent on a conserved motif and provided new insight into the regulatory mechanisms of bifunctional transcription factors in modulating distinct developmental processes. |
