As we report here in PDR1 OE plants, larger epidermal cells or rounder leaves were previously reported in A. thaliana max2 mutants and in ramosus‐1 (rms) and rms‐2 mutants in P. sativum (Beveridge et al., 1997; Stirnberg et al., 2002). Impaired SL activity, either by knocking out SL receptors or biosynthetic genes, or by enhanced SL exudation into the soil, seems to affect leaf development in a similar manner. Despite the lower SL concentrations we detected in PDR1 OE leaves via the parasitic weed germination assay, PDR1 OE plants are still inhibited in lateral bud outgrowth (Sasse et al., 2015), a phenotype known to be mimicked by applications of GR24 on dormant buds (Gomez‐Roldan et al., 2008). At present, no reliable system is available to quantify SL in certain small tissues, such as lateral axils or nodes, where pPDR1:GUS was shown to be expressed (Kretzschmar et al., 2012), or in internal tissues such as the procambium, where cell division is induced by GR24 (Agusti et al., 2011). So we cannot track whether the SL exported from the leaf via PDR1 accumulates into the stem axils or nodes. We suggest that PDR1 overexpression has different, local effects in shoot tissues, probably because of different SL transport routes and/or different locations of the SL biosynthetic pathway. It was reported that PhCCD7 is strongly expressed in stems (Drummond et al., 2015), while PhMAX1, AtD14 and AtMAX1 (Booker et al., 2005; Drummond et al., 2011; Chevalier et al., 2014) are also present in leaves. The SL source and sink map therefore appears to be tissue‐specific; based on our results, we propose the leaf‐to‐stem route as a new SL transport route that is important in the regulation of SL concentrations in leaves and stems. The function of this route seems to be the regulation of leaf senescence, which is SL‐dependent (Ueda & Kusaba, 2015), but it might also contribute to the SL‐driven inhibition of lateral bud growth.