We then compared SL transport in wild‐type, PDR1 OE and pdr1 ko leaves by quantifying leaf loading and unloading of a radiolabeled SL‐mimicking molecule (3H‐GR24) and we compared leaf senescence, a known SL‐related phenotype (Figs 5b, S3b). Leaves were first incubated for 12 h in 1/2 MS + 3H‐GR24 and then transferred in cold 1/2 MS for an additional 10 h. 3H‐GR24 concentrations were scored after leaf loading and unloading. Wild‐type leaves released 26% (± 1.2%) of the loaded 3H‐GR24, while pdr1 ko only released 18% (± 1.3%); PDR1 OE leaves released 46% (± 7.9%), while their wild‐type counterpart only released 32% (± 0.2%). No differences or opposite trends were scored in control transport experiments with tritiated water (Figs 5c, S3c). These results indicate that PDR1, and not transpiration or phloem flows, regulates SL transport out of the leaves. To test if GR24 and not its metabolites are exported from the leaf via PDR1, we directly quantified GR24 leaf loading and unloading via LC‐MS‐MS analyses (see Methods S1; Fig. S4a,b). The results showed GR24 stability in this time span, as also shown by Akiyama et al. (2010) and that the conditions of this experiment produced no detectable (below our detection limits) GR24 degradation products such as the ABC moiety or the hydrolyzed D‐ring (Fig. S4c,d), thus confirming the positive role of PDR1 in GR24 leaf export. Last but not least, we quantified senescence in PDR1 OE, pdr1 ko and wild‐type leaves by visual examination, gene expression analysis and LC‐MS of nonfluorescent Chl catabolites (NCCs) (Berghold et al., 2004; Christ et al., 2016). Three months after germination, P. hybrida leaves were collected and compared. Wild‐type leaves showed senescence from the 11th top leaf down (leaf −11), while in PDR1 OE, leaf senescence started being visible in marginal spots of the leaf blade in the 15th leaf from the top (leaf −15) (Fig. 5d). Leaves of pdr1 ko plants were significantly smaller than the relative wild‐type background (Fig. S3d,e) and started senescing between leaf −11 and leaf −14, at which point the wild‐type showed no senescing leaves. The gene expression of P. hybrida ORE1‐like, SENESCENCE‐ASSOCIATED GENE 12‐like (SAG12like) and SAG13‐like indicators of leaf senescence (Lohman et al., 1994; Breeze et al., 2011) confirmed that senescence emerges earlier in the wild‐type than in PDR1 OE plants, in leaves not showing wilting phenotypes (Fig. 5e,f). In the older leaves −15/−16 (Fig. 5g) the three genes were strongly up‐regulated in the wild‐type but significantly different only for ORE1like and SAG12like. Leaves −11 and −14 from pdr1 ko plants showed an inverted behavior of the SL‐biosynthetic‐ and senescence‐related genes that we found deregulated in PDR1 OE leaves (Fig. S3f,g). MS analyses conducted on the same tissues confirmed the accumulation of NCC 806 and NCC 892 in wild‐type but not in PDR1 OE leaves (Fig. S5a–d). These results show that PDR1 OE leaves can export to the stem more SL than can the wild‐type, thus releasing MAX1 and DAD1 expression from the SL negative feedback and strongly postponing leaf senescence. Also, with the opposite results from the parallel analyses on pdr1 ko plants, we propose that PDR1 regulates the transport of SL out of the leaves, either to the lateral buds or to the main stem.