Source-Sink Relationships
Why does a growing potato tuber, buried in darkness underground, swell with starch? Meanwhile the leaves above ground stay lean and green. The answer lies in one of the most elegant logistical problems solved by plants. They must decide where sugar should come from and where it should go. Every plant runs a constant internal economy. It moves photosynthetic products from the leaves that make them. These products travel to the roots, fruits, seeds, and buds that need them. This chapter explains how plants define, sense, and dynamically re-negotiate the identity of "source" and "sink" tissues. It also shows how phloem loading and unloading mechanisms make the Pressure-Flow Model of Phloem Transport physiologically meaningful. The concept matters because source-sink relationships determine crop yield. They explain why removing flowers can make a plant grow bushier leaves. They also reveal why a shaded branch on a tree can starve even while the rest of the canopy thrives. Agronomists breed crops explicitly to shift the source-sink balance. Modern high-yield wheat and rice varieties are, in large part, plants that have been re-engineered to be better sinks for grain. Understanding source-sink physiology also explains phenomena as diverse as autumn leaf senescence and girdling experiments. It also explains why sugar accumulates in some fruits only after a stone or embryo starts developing. This article builds directly on the pressure-flow mechanism. Source and sink are the two ends of the osmotic gradient that drives mass flow. Here we go one level deeper. We ask how a leaf mesophyll cell gets sucrose into the phloem in the first place. We ask how a root or seed coat pulls it back out. We also ask how the whole system is regulated so that sinks compete for a limited common resource. We will look at the classic experiments that turned "source" and "sink" from vague botanical metaphors into a rigorous, testable physiological framework. These include radiolabeled tracer studies, girdling and defoliation experiments, and studies of the SWEET and sucrose transporter families.
- Source tissues (mature leaves) are net exporters of sugar; sink tissues (roots, fruits, seeds, young leaves, tubers) are net importers.
- Source/sink status is not fixed by anatomy alone — it is a physiological state defined by the direction of net sugar flux, and it can change over a tissue's life.
- Phloem loading at the source concentrates sucrose in sieve elements, either via the apoplastic route (membrane transporters, especially SWEET efflux + SUC/SUT proton-coupled uptake) or the symplastic/polymer-trap route (plasmodesmata + raffinose-family oligosaccharide synthesis).
- Phloem unloading at sinks reverses this logic — sucrose exits sieve elements symplastically or apoplastically and is metabolized, hydrolyzed, or stored, keeping sink solute potential low.
- Sinks compete for photosynthate according to sink strength (size × activity); this competition is measurable and manipulable (defruiting, girdling, shading experiments).
- Whole-plant source-sink balance is a major lever in crop breeding, fruit development, and understanding phenomena like senescence and stress-induced remobilization.
Source and sink are defined not by what an organ is anatomically, but by the direction of net sugar flux across its plasma membranes at a given moment — and it is exactly this flux, sustained by active loading and unloading, that generates the pressure gradient driving phloem mass flow.
The core idea
A source is any plant organ or tissue that produces more sugar (mainly sucrose) than it needs for its own metabolism and growth, so it exports the surplus into the phloem. Mature, photosynthetically active leaves are the paradigm source: net carbon fixers that ship out roughly 50–80% of the sugar they make on a given day. A sink is any organ that consumes or stores more sugar than it produces itself, so it imports sugar from the phloem. Roots, developing fruits and seeds, storage organs like tubers and bulbs, and young expanding leaves are all sinks — even though a young leaf contains chloroplasts and can photosynthesize, it typically imports more sugar than it exports until it reaches roughly 25–40% of its final size, a threshold called the sink-to-source transition. Because this is a physiological rather than a fixed anatomical definition, tissues can switch category over their lifetimes and even over a single day. A young leaf begins life as a sink at its base and a source at its tip (sugar export and import occur simultaneously in different parts of the same expanding leaf), and gradually reverses this as photosynthetic capacity develops from tip to base, ultimately becoming a full net exporter. A storage root is a sink during the growing season and can act partly as a source the following spring, remobilizing stored sugars to fuel new shoot growth. Even mature source leaves can be forced into net sink behavior under extreme shading or during severe carbohydrate deficits, importing sugar from neighboring tissue. The key quantitative concept that ties source and sink together is sink strength, operationally defined as:
where sink size is the total biomass of the importing tissue and sink activity is the rate of import per unit mass (driven by unloading capacity and the rate at which imported sugar is metabolized or converted to storage forms, which keeps solute concentration — and therefore water potential — low inside sink cells). Multiple sinks on the same plant compete for a finite pool of source-derived photoassimilate, and the relative sink strength of each organ determines how much of that pool it captures — this is why removing flowers from a tomato plant redirects sugar into vegetative growth, and why a single dominant fruit can suppress the growth of others on the same truss.
Mechanism
Step 1 — Sugar synthesis in the mesophyll. In a source leaf, The Calvin Cycle fixes CO₂ into triose phosphates in the chloroplast stroma. Triose phosphate is exported to the cytosol via the triose-phosphate/phosphate translocator and converted into sucrose by sucrose-phosphate synthase, ultimately yielding free sucrose (and, in some species, raffinose-family oligosaccharides and sugar alcohols such as sorbitol or mannitol) as the transported sugar. Sucrose is favored as the long-distance transport sugar because it is a non-reducing disaccharide, chemically stable and osmotically "cheap" per carbon delivered, and it does not react non-enzymatically with proteins the way reducing sugars like glucose can.
Step 2 — Phloem loading at the source. Sucrose must move from mesophyll cells, through the bundle sheath, to the minor vein phloem, and finally be concentrated into the sieve element–companion cell (SE-CC) complex, often against a large concentration gradient (source phloem sap sucrose concentrations of 0.3–0.9 M versus mesophyll cytosolic concentrations an order of magnitude lower). Two loading strategies exist, and different species emphasize one or a blend of both:
- Apoplastic loading (dominant in many herbaceous crops, e.g., maize, sugar beet, potato): sucrose diffuses symplastically from mesophyll to the phloem parenchyma, then is actively pumped across the plasma membrane into the cell wall space (apoplast) — this step may involve the SWEET family of sucrose efflux facilitators — and from there is retrieved into companion cells by H⁺/sucrose symporters (SUC/SUT family transporters), powered by the proton-motive force generated by plasma-membrane H⁺-ATPases. This active, energy-dependent step is what allows sucrose to be concentrated in the sieve element well above mesophyll levels.
- Symplastic loading via the polymer trap mechanism (common in many trees and cucurbits, e.g., melon, squash): sucrose moves entirely through plasmodesmata from mesophyll to the specialized intermediary cells adjoining sieve elements, with no apoplastic step. Inside intermediary cells, sucrose is enzymatically converted into raffinose and stachyose — much larger oligosaccharides synthesized from sucrose plus galactinol. Because plasmodesmata connecting intermediary cells to mesophyll are size-restricted, these larger sugars cannot diffuse back out, trapping them in the phloem and maintaining the concentration gradient that drives continued symplastic sucrose influx — an elegant molecular ratchet requiring no membrane transporters at all.
Step 3 — Mass flow. The high solute concentration loaded into source sieve elements lowers the water potential there, drawing water in osmotically from the xylem, and it is exactly this loading-generated turgor pressure that drives bulk (mass) flow of phloem sap toward sinks, as described by the pressure-flow model.
Step 4 — Phloem unloading at the sink. At the sink end, sucrose must exit the sieve elements and be delivered to sink cells, again either symplastically (through plasmodesmata, driven simply by the concentration gradient created by rapid metabolism of sucrose in sink cells) or apoplastically (sucrose effluxes into the cell wall space, often hydrolyzed there by cell-wall invertase into glucose and fructose, which are then taken up by hexose transporters — this is the dominant route in many developing seeds and fruits, where the seed coat/maternal tissue is symplastically isolated from the embryo).
Step 5 — Sink metabolism maintains the gradient. Whatever unloading route is used, the sink cell must keep its internal free-sugar concentration low to sustain continued import — this is achieved by rapid conversion of sucrose into starch (in storage sinks like potato tubers, via ADP-glucose pyrophosphorylase and starch synthase), into structural polysaccharides and respiratory substrates (in growing sinks like root tips), or into vacuolar storage sugars (in many fruits). This continuous metabolic "sink" for sugar is what keeps the sink end of the phloem osmotically dilute and completes the pressure gradient.
The evidence
Radiolabeled ¹⁴CO₂ tracing (mid-20th century onward). The clearest way to prove that a leaf is a source and a fruit or root is a sink is to feed a single leaf ¹⁴CO₂ in a sealed chamber for a short pulse, then track where the label goes over subsequent hours and days using autoradiography or liquid scintillation counting of harvested tissue. Classic experiments of this kind (extending work by researchers such as Mortimer and later refined across many crop species) established two robust patterns that hold across angiosperms: first, label exported from a source leaf moves preferentially to the nearest, most orthostichously connected sinks — an "orthostichy" or vascular-connection effect, since minor veins from a given leaf tend to connect most directly to particular vascular bundles running down the stem. Second, when a competing sink is removed (say, by cutting off a growing shoot tip), the ¹⁴C label previously destined for that sink is redirected to other sinks (axillary buds, roots) within hours, demonstrating that source output is not hard-wired to one destination but is dynamically partitioned according to relative sink strength. This class of experiment converted "source" and "sink" from descriptive labels into an operational, quantitative assay: you can literally count counts-per-minute of radioactivity in every organ and compute the fraction of fixed carbon each sink captures.
Girdling (phloem-ringing) experiments. If a strip of bark (containing the phloem but not the xylem) is removed in a ring around a stem or petiole, sugar transport downward past that point is blocked while water transport in the xylem continues unaffected. The classic observation, going back well over a century in orchard and forestry practice and formalized in physiological experiments, is that:
- Sugar (and starch, as measured by iodine staining or direct sugar assay) accumulates above the girdle, in the source leaf and the tissue just above the cut, because it can no longer be exported.
- Tissue below the girdle — roots, in particular — begins to starve, shows depleted starch reserves, and eventually its growth and even respiration rate decline, while
- fruit or seed development above the girdle on the same branch is often enhanced, because the branch's own source leaves no longer share their sugar with the root system and instead concentrate it in the local sink.
This experiment is a direct physical proof of the pressure-flow-dependent source-to-sink transport axis: cutting the phloem, and only the phloem, is sufficient to reroute a plant's entire carbon economy, exactly as predicted if sucrose flows unidirectionally from source to sink through this one tissue.
Defoliation and defruiting experiments (sink-source manipulation). Removing all but one leaf from a plant, or removing all developing fruit from one truss while leaving fruit on another, allows direct measurement of how source supply and sink demand interact. In tomato and soybean, defruiting one inflorescence while leaving another intact on the same plant consistently increases the photosynthetic rate and delays senescence of leaves that subtend the remaining fruit truss, and it increases seed/fruit size on that truss — direct evidence that sink demand (via unidentified but well-documented "feedback" signals, likely involving sugar-sensing pathways such as trehalose-6-phosphate and hexokinase signaling) feeds back to regulate source photosynthetic capacity itself, not just the direction of transport. This established the important, non-obvious point that source activity is not autonomous — sink demand can up- or down-regulate the rate of photosynthesis in the source leaf, a phenomenon called sink limitation or, when sugars build up because sinks cannot keep pace, feedback (end-product) inhibition of photosynthesis, in which accumulating leaf starch and sucrose down-regulate Calvin-cycle and photosynthetic gene expression.
Molecular confirmation: SWEET and SUT/SUC transporter mutants. More recent molecular genetic evidence has pinpointed exactly which transporters execute the loading step predicted by the older physiological experiments. Loss-of-function mutants or RNAi knockdowns of SWEET efflux transporters (identified by Chen et al. in 2012 using a heterologous glucose/sucrose-sensor screening system in Xenopus oocytes and yeast) block sucrose efflux from mesophyll into the apoplast, causing sugar to accumulate in source leaves and stunting sink growth, exactly as girdling does but at a defined molecular step. Similarly, antisense suppression of SUC2 (a plasma-membrane H⁺/sucrose symporter) in companion cells of transgenic potato and tobacco severely reduces phloem loading, produces plants with pale, sugar-starved sink organs and sugar-engorged source leaves showing visible chlorotic and necrotic symptoms, and confirms that this single transporter family is rate-limiting for apoplastic loading in these species — a direct molecular-genetic recapitulation of what girdling and tracer studies had shown physiologically decades earlier.
Worked examples
Example 1 — Quantitative partitioning after fruit removal (asymmetric sink manipulation). A soybean plant has two pod-bearing branches, A and B, each normally receiving photoassimilate from a shared pool produced by source leaves at a combined rate of 100 mg sucrose equivalents per hour. Under intact conditions, tracer studies show Branch A (with 20 pods) captures 65% of translocated sugar and Branch B (with 10 pods) captures 35%, roughly proportional to pod number, consistent with sink-size-driven partitioning. Suppose all pods are removed from Branch A. Predict, mechanistically, what happens to (i) sugar delivery to Branch B, (ii) photosynthetic rate of leaves subtending Branch A, and (iii) starch accumulation in Branch A's source leaves. Reasoning: With Branch A's sink strength effectively reduced to near zero, competition for the shared photoassimilate pool falls almost entirely on Branch B. Sugar delivery to Branch B should rise substantially — commonly to 80–95% of total translocated sugar in comparable experiments, since Branch B is now nearly the only remaining strong sink, and its own sink activity may even increase somewhat as more substrate becomes available for pod fill. Meanwhile, leaves subtending the de-podded Branch A now have nowhere local to export their sugar (long-distance phloem connections favor nearby sinks), so sucrose and starch accumulate in those leaves. Within 24–72 hours, feedback inhibition of photosynthesis becomes measurable in Branch A's leaves — net CO₂ assimilation rate typically falls by 20–40% relative to leaves subtending intact pods, and this decline in whole-leaf photosynthesis is one of the best-documented examples of sink control over source activity, corroborating both the defruiting experiments and the SWEET/SUT transporter feedback data described above. This demonstrates numerically that "sink strength" is not merely descriptive — it is the quantitative variable that predicts both partitioning percentages and source physiological response.
Example 2 — Osmotic calculation across the loading step (physiological calculation). A mesophyll cell's cytosolic sucrose concentration is 50 mM. Phloem sieve-element sap sucrose concentration at the source, measured by aphid stylectomy (severing an aphid's feeding stylet while it is inserted into a sieve element, allowing pure phloem sap to exude, a technique pioneered in the 1950s–60s), is 0.6 M. Assume T = 293 K (20 °C) and that sucrose is the dominant solute contributing to the osmotic potential difference relevant to loading. Calculate the solute (osmotic) potential contributed by sucrose in each compartment, and comment on what this implies about the loading mechanism. Reasoning: Using (van 't Hoff approximation, i = 1 for a non-ionizing solute like sucrose, R = 0.00831 L·MPa·mol⁻¹·K⁻¹): Mesophyll cytosol: MPa Sieve element: MPa The sieve element is roughly 12-fold more concentrated in sucrose than the mesophyll cytosol, and its solute potential is about 1.3 MPa more negative. Because solutes always diffuse down their concentration gradient, sucrose cannot enter the sieve element passively from the mesophyll side — this large, unfavorable gradient is direct thermodynamic proof that loading must be an active, energy-requiring process, consistent with the H⁺/sucrose symporter mechanism (which uses the proton-motive force established by ATP-driven H⁺-ATPases to co-transport sucrose against its own gradient). This calculation is essentially the quantitative backbone of why phloem loading was long suspected — and later confirmed — to be active rather than a simple diffusive "leak" into the phloem stream.
Common misconceptions & traps
| Misconception | Why it's wrong |
|---|---|
| "Source and sink are fixed anatomical categories — leaves are always sources, roots are always sinks." | Status is physiological and dynamic: young leaves are sinks, mature leaves can become sinks under stress, and storage roots can act as sources during regrowth. |
| "Sucrose moves from source to sink by simple diffusion down its concentration gradient the whole way." | Only the mass-flow step through sieve tubes is a bulk (pressure-driven) flow; loading into and unloading out of sieve elements often requires active transport against strong local gradients (see the osmotic calculation above). |
| "All species load phloem the same way (via transporters)." | Many species (e.g., cucurbits) use an entirely symplastic polymer-trap mechanism with no membrane transporters involved in the loading step itself. |
| "The plant's total photosynthetic output determines sink growth in a simple, one-directional way." | Sink demand feeds back to regulate source activity too — feedback inhibition of photosynthesis and altered gene expression occur when sinks can't keep pace with source supply. |
| "Bigger sinks always win the competition for sugar." | Sink strength depends on activity as well as size; a small, metabolically very active sink (e.g., a rapidly filling seed) can outcompete a larger but sluggish one. |
The scientist behind it
Much of the conceptual and experimental foundation for source-sink physiology, and for the pressure-flow model it depends on, traces back to Ernst Münch, the German plant physiologist who first proposed mass flow driven by osmotically generated pressure gradients in 1930. But the specific experimental toolkit that let physiologists actually measure source-sink fluxes — aphid stylectomy for pure phloem sap sampling, and radiolabeled tracer partitioning studies — developed later through the mid-20th century, largely through the work of plant physiologists studying aphid feeding behavior (notably Tom Kennedy and Charles Mittler in the 1950s–60s, who pioneered using the aphid stylet as a natural, undamaged micro-cannula into single sieve elements) and biochemists mapping sucrose transporter genes in the 1990s–2000s (including Norbert Sauer and colleagues, who cloned and characterized the first plant SUC/SUT sucrose transporters, and Li-Qing Chen, Wolf Frommer, and colleagues, who identified the SWEET transporter family in 2010–2012). Together this lineage transformed source-sink relationships from a descriptive, almost agronomic vocabulary into a molecularly and biophysically grounded field.
Origins · 1 minErnst Münch and how this was discovered
Where this matters today
Crop yield improvement. The "Green Revolution" dwarf wheat and rice varieties of the 1960s worked partly by shifting source-sink balance: shorter stems meant less carbon diverted to structural growth, leaving more photoassimilate for the grain sink, and modern breeding continues to target harvest index (the fraction of total biomass partitioned to the harvested sink organ) as a primary yield lever.
Genetic engineering of sink strength. Researchers manipulate SWEET and invertase gene expression to engineer larger or stronger sinks — for example, enhancing cell-wall invertase activity in developing seeds to increase sink strength and seed size, or exploiting the fact that several plant pathogens (notably Xanthomonas bacteria causing bacterial blight in rice) hijack SWEET transporters to divert host sugar to feed the pathogen, making SWEET genes an active target for disease-resistance breeding.
Fruit and vegetable quality. Postharvest physiologists manipulate source-sink dynamics before harvest (via pruning, girdling, and defruiting practices) to concentrate sugars in fewer, larger fruit — a direct commercial application of the girdling experiments described above, used routinely in viticulture and orchard management to boost fruit sugar content (Brix) at harvest.
Stress physiology and remobilization. Under drought or nutrient stress, understanding which organs act as temporary sources (remobilizing stored carbon and nitrogen from stems and leaves) versus sinks (developing grain) helps explain and predict yield losses, and informs breeding for stress-resilient carbon allocation.
Conservation and forestry. Source-sink carbon allocation models underlie predictions of how trees respond to defoliation by insects, partial canopy loss, or changing light environments, informing forest management and models of ecosystem carbon storage under climate change.
Ask the tutor: How does the trehalose-6-phosphate signaling pathway link sugar status to sink strength and flowering time?
Is a source always a leaf, and a sink always a root or fruit?
No. Source and sink describe a physiological role — net sugar exporter versus net sugar importer — not a fixed anatomical identity. Most mature, fully expanded, photosynthetically active leaves are sources, and most roots, fruits, seeds, and young leaves are sinks, but exceptions are common and instructive. A germinating seed's endosperm or cotyledon is a source, mobilizing stored reserves to feed the growing embryo, which is the sink. A storage root or bulb switches from sink (accumulating reserves) to source (remobilizing them to fuel new shoot growth) seasonally. Even a mature leaf can behave as a transient sink if heavily shaded and unable to meet its own respiratory needs, importing sugar from better-lit neighbors. The defining test is always the net direction of sugar flux at that moment, not the tissue's identity or developmental stage in the abstract.
Why does phloem loading need to be "active" if pressure-flow itself is passive?
Pressure-flow describes movement within the sieve tube system — sap flows from high to low hydrostatic pressure, which is a passive, physical process requiring no additional metabolic input along the way. But generating that pressure difference in the first place requires concentrating sucrose in source sieve elements far above the concentration present in surrounding mesophyll cells, and diffusion alone cannot move a solute against its own concentration gradient. This concentrating step — apoplastic loading via H⁺/sucrose symporters powered by ATP-driven proton pumps, or symplastic loading coupled to raffinose synthesis that traps sugar against back-diffusion — is the genuinely active, energy-requiring part of the system. Without active loading (and active or facilitated unloading at the sink, which removes sugar from the sieve tube and keeps the sink end dilute), there would be no pressure gradient for mass flow to passively follow.
What is "sink strength" and how is it measured experimentally?
Sink strength is operationally defined as sink size multiplied by sink activity — the total capacity of an organ to attract and use photoassimilate. It is measured experimentally in several converging ways: by feeding a source leaf ¹⁴CO₂ and tracking the fraction of radiolabel that accumulates in each competing sink over time; by comparing growth rates or dry-matter accumulation of sinks before and after removing a competitor (defruiting or defoliation experiments); and by directly assaying unloading capacity, for example measuring cell-wall invertase activity or sucrose transporter expression in the sink tissue itself. A sink with high activity (rapid metabolism of imported sugar, keeping internal concentration low) can outcompete a physically larger but metabolically sluggish sink, which is why sink strength — not sink size alone — is the physiologically meaningful variable.
How does girdling prove that phloem, not xylem, carries sugar?
Girdling removes a ring of bark, which contains phloem (and cork, cortex) but leaves the xylem-containing wood intact, so water and mineral transport upward continue unaffected. If sugar were transported via the xylem, girdling should have no effect on sugar distribution. Instead, girdling reliably causes sugar and starch to accumulate above the cut (in source tissue that can no longer export) and causes starvation, growth arrest, and eventual death of tissue below the cut (roots and stem tissue that depend on imported sugar). This selective, phloem-specific disruption with a very specific and predictable pattern of accumulation versus starvation is strong physical evidence that sugar transport is a phloem-specific, not xylem-mediated, process — a conclusion later reinforced at the molecular level by phloem-specific transporter mutants that reproduce the same phenotype.
Can a single organ switch between being a source and a sink within its own lifetime?
Yes, and this is one of the clearest demonstrations that source/sink status is physiological rather than fixed. A developing leaf begins entirely as a sink, importing sugar to fuel cell division and expansion. As chloroplasts mature and photosynthetic capacity rises, the leaf's own sugar production begins to exceed its needs, and it transitions to net export — the sink-to-source transition — typically once the leaf reaches roughly 25–40% of its final area, progressing from leaf tip (which matures first) toward the base. Similarly, storage organs like potato tubers or bulbs act as sinks while accumulating starch during one growing season, then act partly as sources the following season, mobilizing stored carbon to support new sprout growth before new leaves become photosynthetically self-sufficient.
Why do some plant pathogens target SWEET transporter genes?
Because SWEET transporters control the efflux of sucrose out of plant cells — the very step that supplies sugar to the phloem at sources and to growing tissue at sinks — they represent an attractive resource for pathogens seeking a free carbon supply. Certain strains of the bacterium Xanthomonas oryzae, which causes bacterial blight in rice, secrete transcription-activator-like (TAL) effector proteins that bind rice SWEET gene promoters and induce their overexpression specifically at the site of infection, causing the plant to leak sucrose into the apoplast where the bacteria feed on it — effectively hijacking a normal source-sink transport gene for pathogen nutrition. This discovery has made SWEET promoter regions and coding sequences an active target in breeding disease-resistant rice varieties, since disrupting the TAL-effector binding site can block this sugar hijacking without impairing normal phloem loading.
Does removing flowers or fruit from a plant really make it grow more leaves and roots?
Yes, and this is a direct, reproducible consequence of source-sink competition. Flowers and developing fruit are typically very strong sinks — often the strongest on the plant, because seed and fruit tissue metabolizes imported sugar rapidly to fuel high rates of cell division, starch or oil deposition, and structural growth. When these sinks are removed (as in commercial practices like flower/fruit thinning, or simply deadheading ornamental plants), the photoassimilate that would have gone to them is redirected to the remaining sinks — typically vegetative meristems, roots, and any remaining fruit — increasing vegetative growth, root biomass, or the size of remaining fruit. This is precisely why gardeners deadhead flowers to promote leafy growth and why orchardists thin young fruit to increase the size of those that remain.