How Do Stomata Close in Response to Vapor Pressure Deficit?

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How do stomata close in response to vapor pressure deficit? When the air draws more water out of a leaf, the pores on the leaf surface shut to slow that loss. Vapor pressure deficit, or VPD, measures how strongly the air pulls water from plants. Two sources explain the mechanism. One covers the molecular signals behind the closure, and the other traces how the response changed across plant groups. The steps below follow the answer in order.

Quick answer

  • Vapor pressure deficit is the difference between saturation and actual air vapor pressure, and it indicates the level of atmospheric drought and evaporative pressure on plants.
  • Rising VPD induces stomatal closure to counteract the VPD-mediated evaporative water loss from plants.
  • In ferns and conifers, the closure is described as a passive hydraulic process that does not depend on ABA.
  • In angiosperms, a rapid increase in foliar ABA concentration preceded stomatal closure, so ABA is the main signal in those plants.

What VPD measures

The first source defines the term directly. Vapor pressure deficit (VPD), the difference between the saturation and actual air vapor pressures, indicates the level of atmospheric drought and evaporative pressure on plants. A higher VPD means a stronger pull on the water inside the leaf.

The source explains what the plant does in response. VPD is the measure of evaporative potential, and its increase causes higher transpiration from plants, followed by stomatal closure to reduce excessive water loss. Transpiration is the loss of water from the leaf, and closing the stomata is the response that limits it.

The second source describes the same pattern across plant groups. It states that stomatal responses to vapor pressure deficit are a principal means by which vascular land plants regulate daytime transpiration. It also notes that stomata typically close at high VPD and open at low VPD. That pattern is the basic answer to the question. The mechanism is what the sources spend most of their text explaining.

Why the air matters

The first source explains why VPD has been rising. VPD increases during climate change due to changes in air temperature and relative humidity.

The second source adds that the mechanism for the stomatal response to VPD remains poorly understood. Researchers have explored a range of hypotheses. One extreme holds that stomata respond passively through changes in leaf water content induced by the VPD or humidity perturbation. The other holds that stomata close uniquely in response to the plant hormone abscisic acid. The sources present these as competing views, not as settled facts.

Mechanism one: passive hydraulic closure

The passive route depends on water status inside the leaf. In these basal vascular plants, reductions in leaf water potential and leaf and guard cell turgor pressure were reported to directly promote stomatal closure in response to high VPD. The second source adds that stomata open and close by changes in guard cell turgor. In this account, the guard cells do not need a hormone signal to close.

The first source describes the process in ferns and conifers. VPD-induced stomatal closure was reported to be a passive-hydraulic ABA-independent process in ferns and conifers. The second source says that the stomata in basal lineages of vascular plants, including gymnosperms, appeared to respond passively to changes in leaf water status induced by VPD perturbation. Both sources place this route in the older plant lineages.

The passive route also has a timing effect. Upon an increase in VPD, a rapid rise in transpiration results in reduced epidermal turgor and in less backpressure on the guard cells. The first source notes that this promotes a transient passive opening.

Mechanism two: ABA signaling

The active route uses abscisic acid, a plant hormone. For the active process, ABA was proposed to be involved for two reasons. A rapid increase in foliar ABA concentration preceded stomatal closure, and VPD-induced stomatal closure was absent in ABA-deficient mutants. The first source reports the timing of the signal. A rapid, within 10 minutes, VPD- or turgor-induced increase in foliar ABA concentration preceded stomatal closure.

The speed of the response is one reason the ABA route is studied closely. The half-response time of high VPD-induced stomatal closure was short.

The second source makes the same point about angiosperms. In contrast, foliar ABA appeared to drive the stomatal response to VPD in the angiosperm samples. Increased foliar ABA level at high VPD in angiosperm species resulted in hysteresis in the recovery of stomatal conductance. In other words, the stomata reopen more slowly than they closed. The source adds that this was most pronounced in herbaceous species.

How the two routes fit together

The second source frames the difference as an evolutionary change. The mechanism for a stomatal response to vapor pressure deficit evolved from a passive regulation in basal vascular plants to mediation by ABA in the earliest angiosperms.

The data in the second source show the difference clearly. In the six diverse fern and conifer species, the rate of stomatal closure during a VPD transition from 0.7 to 1.5 kPa was the same as that for stomatal opening when the original VPD was restored. In contrast, in the two herbaceous angiosperm species, the rate of stomatal closure at high VPD was much greater than the rate of stomatal opening on returning to low VPD.

The first source adds that the role of ABA is still disputed. The involvement of ABA in VPD-induced stomatal regulation is controversial. It also notes that currently it is unclear whether angiosperms can display passive hydraulic stomatal closure, which leaves the answer for those plants open.

For a broader view of stomatal opening and closing, see how stomata open and close. For how plants handle another kind of stress that changes water status, see how cold hardiness works in plants.

How we chose

The two sources were chosen because each covers the mechanism of stomatal closure in response to VPD. The first covers molecular regulation, including ABA-dependent and ABA-independent components. The second covers the evolution of the response across vascular land plants and measures ABA levels and stomatal conductance. Both are hosted on PubMed Central, and neither is a retail page.

What we could not verify

The sources do not settle the mechanism in every plant. The first source states that there are important gaps in our understanding of the molecular VPD sensing and signalling mechanisms in stomatal guard cells. The gaps it lists include which components are involved in the ABA-independent regulation of OST1 and whether OST1 activation above basal activity is needed for VPD responses.

What the sources do not say

The sources describe mechanisms and measurements in Arabidopsis and in the wider vascular plant groups. They do not give a closure rate for a particular crop or houseplant under a particular afternoon. The second source notes that very few studies have quantified changes in ABA level in response to VPD, so the amount of ABA needed for closure in any given plant is not stated in these two sources.

Frequently asked questions

What does vapor pressure deficit mean for a leaf?

It is a measure of evaporative pressure on the plant. The first source defines VPD as the difference between the saturation and actual air vapor pressures, and it links that difference to the level of atmospheric drought. A higher VPD increases the pull on the leaf’s water.

Do all plants close their stomata the same way?

The sources describe two routes. The second source says the mechanism evolved from a passive regulation in basal vascular plants to mediation by ABA in the earliest angiosperms. Ferns and conifers respond through passive water status, while angiosperms show a stronger ABA role.

Is ABA always needed for stomatal closure?

The sources do not say that it is always needed. The first source reports that VPD-induced stomatal closure was reported to be a passive-hydraulic ABA-independent process in ferns and conifers. For angiosperms, the involvement of ABA is described as controversial.

Why can stomata open briefly when VPD rises?

The first source describes a transient passive opening that follows a rise in transpiration. That short movement is followed by stomatal closure in the source’s account of the response.

Why are stomata slower to reopen than to close?

The second source reports hysteresis in angiosperms. Increased foliar ABA level at high VPD in angiosperm species resulted in hysteresis in the recovery of stomatal conductance, and this was most pronounced in herbaceous species. The stomata close quickly but recover more slowly.

Sources

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