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![]() Although this change in PD transport as leaves age has been recognized for several decades, little is known about how PD transport between cells is coordinated with leaf development and physiology during the sink-to-source transition. In contrast to source leaves, PD transport is unrestricted in young sink leaves, which allows rapid, passive transport of sugars out from the vasculature into the growing leaf ( 27 – 29). Phloem loading has a dual effect: The concentration of solutes in the phloem increases, creating hydrostatic pressure that can promote phloem transport, and perhaps more importantly, the concentration of free sugars in the source leaf is reduced (i.e., export of photo-assimilated carbohydrates from the source to growing sink tissues is maximized) ( 26). To prevent passive backflow of sugars from the vasculature into the leaf, PD transport is tightly restricted in source leaves ( 1). In source leaves of apoplastic loaders, sugars are loaded against a concentration gradient into the phloem companion cells by active transporters in the plasma membranes ( 22 – 25). Among different plant species, there is considerable variation in how sugars are loaded from the photosynthetic mesophyll into the phloem here, we will focus on herbaceous plants, which typically use an “apoplastic” loading mechanism. As leaves develop, they switch from importing nutrients out from the phloem (sinks) to exporting sugars into the phloem (sources), a physiological shift that is called the “sink-to-source” transition. Tracheophytes traffic sugars via the phloem, specialized vascular tissue that concentrates high levels of sugars for long-distance transport through the plant body. PD transport is also tightly regulated during various stresses, especially upon recognition of infection by a pathogen ( 5, 17 – 21).ĭuring plant development, plants redistribute sugars photosynthesized in mature leaves (“sources”) to support the development of young leaves and roots (“sinks”). When plants undergo developmental transitions, such as during lateral root formation, PD transport is often restricted, which is proposed to isolate cells during differentiation and allow signaling molecules (such as phytohormones and transcription factors) to accumulate to high concentrations ( 3, 12 – 16). We and others discovered that chloroplasts can regulate the rate of PD transport and the biogenesis of PD in pathways that we named “organelle-nucleus-plasmodesmata signaling” ( 6 – 11). The upstream signal transduction pathways that regulate PD transport in plants remain poorly understood, however. PD are absolutely essential for plant development and physiology, and their importance is reflected in the repeated, parallel evolution of PD or analogous structures in every lineage of complex multicellular eukaryotes that have cellulosic cell walls ( 4, 5). Plant cells are connected by plasmodesmata (PD), nanoscopic membrane-bound channels in the cell wall that permit molecules up to ∼80 kDa to traffic between neighboring cytoplasts ( 1 – 3). ![]() We conclude that leaf cells regulate PD trafficking in response to changing carbohydrate availability monitored by the TOR pathway. We further found that TOR is significantly more active in mature leaves photosynthesizing excess sugars than in young, growing leaves, and that this increase in TOR activity correlates with decreased rates of PD transport. Genetic approaches and chemical or physiological treatments to either promote or disrupt TOR activity demonstrate that glucose-activated TOR decreases PD transport in leaves. From a forward genetic screen for altered PD transport, we discovered that the conserved eukaryotic glucose-TOR (TARGET OF RAPAMYCIN) metabolic signaling network restricts PD transport in leaves. Although fundamental to plant physiology, the mechanisms that control PD transport and thereby support development of new leaves have remained elusive. ![]() The coordinated redistribution of sugars from mature “source” leaves to developing “sink” leaves requires tight regulation of sugar transport between cells via plasmodesmata (PD). ![]() This act established daylight saving from the last Sunday in April to the last Sunday in October. 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