The overexpression of PDR1 in P. hybrida plants was previously reported to inhibit shoot lateral branching (Sasse et al., 2015). This result raised the question of whether PDR1 OE plants might increase not only SL transport but also its synthesis. Our results show that SL biosynthesis genes are induced in PDR1 OE roots and shoots, indicating that there is a cross‐regulation between transport and biosynthesis. We hypothesize that the higher amounts of SL transported from the root tip into the soil in PDR1 OE plants release DAD1 and MAX1 from a negative feedback regulation, which might occur in the presence of inhibitory concentrations of SL, thus allowing a higher biosynthesis of SL in shoots and roots. However, this does not necessarily cause higher SL concentrations in all tissues: SL could be even lower, probably because of simultaneously increased transport/export as seen for roots and leaves (see Fig. 9). DAD1 also fits this model in pdr1 ko leaves: it is strongly down‐regulated where SL accumulates. The nonresponsive behavior of MAX1 in pdr1 ko leaves is probably a result of the senescence of pdr1 ko leaves, as MAX1 was reported to be up‐regulated by senescence (Ueda & Kusaba, 2015). PDR1 OE stems seem to diverge from this theory, as stems are low in SL, but also in MAX1 and DAD1. Still, PDR1 OE shoot lateral branching is strongly delayed (Sasse et al., 2015), as if, close to lateral buds, SL concentrations and/or transport are still high enough to inhibit bud outgrowth. Alternatively, the PDR1 OE‐originated redistribution of SL creates plants that are more susceptible to SL in targeted areas such as dormant buds, which might be regulated by the SL ratio between nodes/internodes rather than by the total amount of SL in the stems. It is possible that more sensitive ways of quantifying SLs would allow a finer map of SL distribution in nodes and internodes to be drawn, thus allowing us to understand if local peaks of SL synthesis and distribution are responsible for the regulation of shoot lateral branching. ABC transporters are known to be frequently induced by their substrates (Hwang et al., 2016); however, to our knowledge it has not yet been shown that ABC transporters affect the synthesis of their substrates similarly.