Do Stomata Open or Close in Heat?—How Plants Balance Water and Cooling

On a hot day, should a plant open its stomata or close them?

Many people first learn that plants close stomata to avoid losing water. That is true—but it is only part of the story. By opening stomata and allowing water to evaporate from leaves, plants can also dissipate heat through transpirational cooling. The physical principle is similar to sweating in animals: evaporation consumes heat.

So which response is correct in heat—opening or closing?

Recent work suggests that the question itself is too simple. Plants are not following a single rule such as “heat means open” or “heat means close.” To cool a hot leaf, opening is useful. To conserve water, closing is useful. Light, atmospheric dryness and the plant’s internal water status add further inputs.

The final stomatal aperture is therefore better understood as the outcome of competing demands rather than a binary switch.

A study published in Nature Plants on August 26, 2026, adds a new molecular branch to this regulatory network. When that discovery is connected with several recent studies, a broader picture emerges of how plants balance heat dissipation against water conservation.

A newly identified pathway that promotes stomatal opening at high temperature

The central protein in the new study is UBP24.

UBP24 stands for UBIQUITIN-SPECIFIC PROTEASE 24. It is a deubiquitinating enzyme: a protein that removes ubiquitin from other proteins.

Ubiquitin is a small protein that can be attached to cellular proteins and alter their stability, trafficking or degradation. By removing ubiquitin, UBP24 can change how long a target protein remains functional and where it is maintained in the cell.

The new study shows that high temperature activates B4 RAF-like kinases, a group of protein kinases, which in turn activate OST1 (OPEN STOMATA 1, also called SnRK2.6).

OST1 then phosphorylates UBP24 at serine 360 (Ser360). Phosphorylation is the addition of a phosphate group to a protein and is one of the most common ways cells alter protein activity, stability, interactions and charge.

Phosphorylation at Ser360 stabilizes UBP24. UBP24 then removes ubiquitin from AHA1 (ARABIDOPSIS H+-ATPASE 1), a proton pump located in the plasma membrane. This suppresses AHA1 internalization and degradation, allowing more AHA1 to remain at the membrane.

The pathway can therefore be simplified as:

high temperature → B4 RAF-like kinases → OST1 → UBP24 → maintenance of AHA1 at the plasma membrane → stomatal opening

AHA1 is part of the machinery that physically drives stomatal opening

Understanding AHA1 makes the new pathway much easier to visualize.

A stoma is bordered by a pair of guard cells. When guard cells accumulate solutes and take up water, their turgor rises and the pore opens. When they lose solutes and water, turgor falls and the pore closes.

Plasma-membrane H+-ATPases such as AHA1 use energy from ATP to pump protons (H+) out of guard cells. This hyperpolarizes the plasma membrane, facilitating the uptake of potassium ions (K+) and other osmotic solutes. Water follows osmotically, guard-cell turgor increases, and the stomatal pore opens.

AHA1 is therefore an important component of the opening machinery.

What makes the new result especially interesting is that AHA1 had already appeared in another recent high-temperature study.

A 2025 Nature Plants paper showed that TOT3 (TARGET OF TEMPERATURE 3), a temperature-responsive kinase, phosphorylates plasma-membrane H+-ATPases including AHA1 and increases their activity, promoting stomatal opening at high temperature.

That earlier work identified a mechanism that effectively says:

activate AHA1.

The 2026 UBP24 study adds another layer:

keep AHA1 at the membrane.

The same downstream opening machinery is therefore regulated both through its enzymatic activity and through protein stability and localization.

Why, then, do plants also close stomata in hot and dry conditions?

This brings us back to the apparent contradiction.

If opening stomata helps cool leaves, why do plants often close stomata during hot, dry weather?

The key is to separate temperature from atmospheric and soil water status.

Warm air can hold more water vapor than cool air. If the actual amount of water vapor does not increase proportionally as temperature rises, the atmosphere becomes more effective at drawing water from leaves.

A common measure of this drying power is VPD, or vapor pressure deficit. VPD is the difference between the amount of water vapor the air could hold at saturation and the amount it actually contains. A larger VPD generally means a stronger evaporative demand on the leaf.

In many plants, stomatal conductance declines as VPD rises. This limits excessive water loss. Soil drought likewise shifts stomata toward closure.

A hot plant can therefore receive at least two opposing pressures:

the leaf is hot → evaporative cooling is valuable → opening is favored

but at the same time:

the air is dry or soil water is limited → water loss is dangerous → closing is favored

Temperature can increase the need for cooling while also increasing evaporative demand. The two effects need not point in the same direction.

A 2026 review in New Phytologist emphasizes precisely this distinction: direct temperature effects on guard cells must be separated from indirect effects caused by temperature-dependent changes in VPD and plant water status.

Is there really a temperature-driven opening response independent of drought?

This requires an important fact check.

One could argue that apparent responses to heat are merely consequences of changes in humidity or soil drying. Several experiments argue against such a simple explanation, at least in Arabidopsis thaliana.

The TOT3 study analyzed high-temperature-induced stomatal opening and also used isolated epidermal preparations. The new UBP24 study likewise examined peeled leaf epidermis under dark conditions across 21, 28, 35 and 42 °C. In wild-type tissue, stomatal aperture increased at 35 and 42 °C.

These experiments provide evidence that Arabidopsis possesses a temperature-responsive opening mechanism that cannot be explained solely as a secondary consequence of soil drought.

The UBP24 study also tested the role of the plant hormone ABA (abscisic acid) using a guard-cell ABA sensor, inhibition of ABA biosynthesis and genetic approaches. The authors concluded that activation of the high-temperature OST1–UBP24 pathway does not require the conventional increase in ABA associated with drought signaling.

ABA is one of the central hormones of plant water-stress responses. During drought, ABA signaling strongly promotes stomatal closure.

OST1 was classically known as a stomatal-closing kinase

This is where the story becomes particularly interesting.

OST1—OPEN STOMATA 1, also known as SnRK2.6—has long been a central component of ABA-induced stomatal closure.

Under drought and ABA signaling, OST1 activates targets including SLAC1 (SLOW ANION CHANNEL-ASSOCIATED 1), an anion channel in guard cells.

Activation of SLAC1 promotes anion efflux. This changes the membrane potential and contributes to the loss of potassium and other osmotic solutes. Water then leaves the guard cells, turgor decreases, and the stomatal pore closes.

The classical pathway can be simplified as:

ABA → OST1 → SLAC1 → stomatal closure

The TOT3 study added another closing-side action of OST1. Under drought, OST1 phosphorylates and inhibits TOT3.

Because TOT3 normally activates AHA1 and promotes opening, drought-associated OST1 can support closure in two complementary ways:

activate the machinery that closes the pore

and

suppress machinery that would otherwise open it.

The 2026 UBP24 paper now shows the same OST1 kinase participating in the opposite direction under high-temperature conditions: OST1 phosphorylates UBP24, UBP24 stabilizes AHA1, and stomatal opening is promoted.

So OST1 can no longer be thought of simply as a “stomatal closure switch.”

It is better viewed as a signaling junction whose output depends on upstream conditions and downstream targets.

Another study reports OST1-dependent stomatal closure during heat stress

The story is even more complex.

A 2025 Molecular Plant study reported an OST1-dependent pathway that promotes stomatal closure under high-temperature stress in Arabidopsis.

That study focused on HSFA1b (HEAT SHOCK FACTOR A1b), a heat-shock transcription factor.

At normal temperature, HSFA1b is mainly present in the cytoplasm and its adenylate-cyclase activity generates cAMP (cyclic adenosine monophosphate), which suppresses OST1 activity.

At high temperature, HSFA1b relocates to the nucleus. The inhibition of OST1 is relieved, allowing OST1 to activate SLAC1 and promote stomatal closure. The authors proposed this as another ABA-independent heat-response pathway.

The current literature therefore contains both:

high temperature → OST1 → UBP24 → AHA1 → opening

and

high temperature → HSFA1b relocalization → OST1 → SLAC1 → closure

Both have been reported experimentally.

And this means the field cannot be reduced to a simple rule that “ABA means closing, no ABA means opening.” Both of these high-temperature pathways were described as ABA-independent in their respective experimental systems.

This does not mean 34 °C opens stomata and 37 °C closes them

A tempting interpretation would be to arrange the studies by temperature and infer a single threshold: perhaps moderate heat opens stomata and stronger heat closes them.

The available evidence does not justify that conclusion.

The studies differ in treatment duration, light conditions, humidity, VPD, water availability, tissue preparation and whether measurements were made in intact plants or isolated epidermis.

The UBP24 study, for example, observed temperature-induced opening even at 42 °C in its epidermal assay, whereas the HSFA1b study reported closure under its own high-temperature stress conditions.

Temperatures from different experimental systems therefore cannot simply be placed on one universal response curve.

The 2026 New Phytologist review explicitly discusses these apparently contrasting observations. The important unresolved question is which physiological and experimental conditions determine which signaling branch dominates.

The current state of knowledge is therefore:

molecular pathways that promote opening are real, and molecular pathways that promote closure are real—but we do not yet have a complete rule for when each one dominates.

Stomatal aperture may be better understood as the output of competing pathways

The authors of the 2026 Nature Plants paper also explored this problem with a computational model.

The model combines several signaling branches, including the previously described TOT3–AHA1 module, the OST1–SLAC1 closure branch and the newly identified OST1–UBP24–AHA1 branch.

Opening and closing pathways can therefore operate within the same network, while ABA input changes the balance between them.

In Extended Data Fig. 10, the authors simulated stomatal aperture under 21 and 42 °C conditions, with or without ABA-related input.

This provides a useful conceptual shift.

Stomatal behavior is not well described by asking only whether temperature is high or low.

In a real plant, the relevant state is multidimensional, involving at least:

temperature × VPD × plant water status × light × time

Multiple molecular branches respond to those inputs, and their combined strengths determine the final pore aperture.

Stomata are therefore better viewed not as binary ON/OFF switches, but as continuous control systems that integrate multiple environmental signals.

The model is not a finished universal predictor

An important limitation remains.

The computational model in the UBP24 paper is not a complete quantitative predictor of stomatal behavior under every environmental condition.

Detailed kinetic information is still missing for many components, and existing experiments have been performed under different physiological and technical conditions. One central unresolved question is how the same OST1 kinase can generate distinct downstream outputs toward opening or closure.

The model should therefore be viewed as a mechanistic framework—a way to test whether apparently conflicting stomatal responses can emerge from a network containing several competing branches.

Even so, bringing these pathways into a shared network is an important step beyond treating each new molecule as an isolated discovery.

The UBP24 paper also contains an intriguing evolutionary result

The study is not only about stomata.

When OST1 phosphorylates UBP24 at Ser360, the phosphate introduces negative charge at that position. The authors found that this negative charge is important for UBP24 stability and function.

Their evolutionary analysis suggests that regulation involving Ser360 emerged in association with vascular-plant evolution.

The comparison with yeast is particularly striking. The UBP24-related yeast protein Ubp3 contains a constitutively negatively charged amino-acid residue at the corresponding position, and that negative charge is required for growth after heat shock.

Plants can therefore place negative charge at the site transiently through phosphorylation.

Yeast can encode negative charge there directly in the amino-acid sequence.

The organisms and downstream functions are very different, but the study suggests a shared physical principle: the charge state of a specific protein position can be tuned to shape heat responses.

Stomata may be control valves for allocating water, heat and carbon

Read in isolation, the UBP24 paper is a study describing a new pathway for high-temperature-induced stomatal opening.

Placed beside recent work, however, it contributes to a broader model of stomatal regulation.

Opening stomata helps plants take up carbon dioxide and can cool leaves through transpiration—but it also loses water.

Closing stomata conserves water—but restricts carbon dioxide uptake and weakens evaporative cooling.

Neither fully open nor fully closed is always optimal.

Plants must continuously trade among at least three demands:

take up carbon, conserve water, dissipate heat.

Stomata are the adjustable valves through which those demands are negotiated.

The emerging picture is not one sensor controlling one switch. It is a network containing opening and closing branches involving AHA1, TOT3, UBP24, OST1, SLAC1 and other regulators.

OST1 is especially illustrative.

Under drought-associated signaling, it promotes closure.

Under high-temperature conditions, it can promote opening through UBP24.

In another heat-response pathway, it can contribute to closure through SLAC1.

At first glance, that seems contradictory.

But the physiological problem faced by the plant is itself contradictory: it must cool the leaf without losing too much water. A control system containing opposing branches may therefore be exactly what is required.

The new study adds UBP24 as another component of that control network.

Stomata may not be deciding simply whether to open or close.

They may be continuously solving a more difficult problem:

how far should the pore be open under the conditions the plant is experiencing right now?

References

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3. Zhang Y, Song R-F, Hu X-Y, et al. Arabidopsis HSFA1b functions as a heat sensor inhibiting OST1-mediated stomatal closure through its adenylate-cyclase activity. Molecular Plant. 2025;18:1549–1566. DOI: 10.1016/j.molp.2025.07.018
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