Blog myth #2."Hot days permanently break HREZ resistance"

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Blog myth #2."Hot days permanently break HREZ resistance"

Truss tomato on a purple background, with a HREZ sticker on the former to last tomato

Understandable question: does HREZ break on hot days?

One of the most persistent concerns we hear from growers is that high temperatures can “break” ToBRFV resistance — especially in varieties carrying HREZ. This idea comes from the history of older resistance genes like Tm22, which were known to show temperature dependent behavior under certain conditions. During periods of extreme heat combined with high virus pressure, these resistances sometimes appeared to weaken or temporarily lose effectiveness.

So the question is understandable: Does the same apply to HREZ?

Understanding temperature effects on resistance

Temperature can influence how R-gene–mediated resistances behave. In certain wild tomato accessions, researchers observed that resistance to ToBRFV could temporarily weaken at around 33 °C -  but importantly, when temperatures dropped again, the resistance returned.

This is not a permanent breakdown, but a reversible suppression of the plant’s defense response.

And this matters, because even in hot climates, night temperatures typically fall back into the range where the resistance protein is functional to activate a defense response. In practice, this means that temporary suppression during the hottest hours of the day does not automatically lead to ToBRFV problems.

This phenomenon is not unique to HREZ. It’s a well known feature of several resistance proteins, including Tm22. Historical reports from the introduction of Tm22 (Hall, 1980) describe temperature related issues under high virus pressure - very similar to what we sometimes observe with HREZ today.

The key insight is this: The effect becomes critical only when prolonged high temperature is combined with high virus pressure.

Ilse Bakker, Researcher Plant Immunity & R-Gene Stability

“As part of the EU project NEMEMERGE, I study how different resistance proteins respond to heat. Some remain stable, while others cannot optimally activate an immune response at high temperatures. But this effect is reversible — when temperatures drop, the resistance fully returns. The real risk arises when heat coincides with high disease pressure. That’s why understanding heat stability under realworld conditions has become such an important part of our work at Enza Zaden.”

What we learned from early HREZ experience

Before commercial launch, HREZ was tested extensively across regions with warm climates and the results were very positive. However, our first encounter of extreme summer conditions worried us initially. With night temperatures that never dropped below 33 °C and a ToBRFV viral load that grew rapidly, we started to observe strong hypersensitive response. It wasn’t something we had observed in precommercial trials in warm climates where night temperature were dropping below 33 °C.
This experience taught us two important things:

  • HREZ is not uniquely temperature sensitive. Its behavior is comparable to Tm22 when both are exposed to high pressure and heat.
  • High pressure is the real trigger. Today, Tm-22 appears “stable” simply because ToMV pressure in Tm-22 crops is low. Under high pressure, Tm-22 would show similar stress responses.

In other words: “HREZ doesn’t fail simply because it’s hot — the real challenge appears when prolonged high temperatures coincide with high virus pressure, which is when the hypersensitive response becomes visible.”

What growers actually see in practice

Across commercial production in warm regions, HREZ varieties perform well under typical summer conditions. Growers consistently report stable resistance, healthy plants, and good yield — even in climates where temperatures regularly rise above 30 °C. When issues do occur, they almost always coincide with:

  • very high virus pressure
  • compromised hygiene
  • mechanical spread
  • prolonged heat stress

This is not unique to HREZ. It’s how biological resistance systems behave under extreme combined stress.

Gianplacido Di Rosa, Senior Tomato Breeder, Italy

“Our first winter trials in 2022 in Sicily looked perfect — no issues at all. But when summer arrived, with high temperatures and high virus pressure, we immediately observed excessive hypersensitive reactions. That was the turning point. Over the next three years, we tested different genetic backgrounds under these extreme conditions, and that’s how we learned which combinations stay stable in the heat. It wasn’t theory — it was real plants, real pressure, and a lot of field work.”

Nuance matters

It’s important to avoid oversimplifying the story in either direction: ,

  • No, temporary heat induced inactivation of HREZ does not automatically lead to ToBRFV problems. Cooler night temperatures reactivate the resistance mechanism.
  • Yes, extreme prolonged heat combined with high virus pressure can challenge HREZ, just like any R-gene system.

The real world takeaway is straightforward: Under realistic commercial conditions, HREZ remains strong and reliable — even in warm climates — as long as hygiene and pressure management are in place.

What the data shows

A research team from the Hungarian University of Agriculture and Life Sciences and the University of Jordan screened 173 wild tomato accessions and identified several plants with strong natural resistance to ToBRFV (Jewehan et al. 2022). At normal temperatures (22–24 °C), these resistant plants stayed completely symptom-free, and no virus could be detected in either inoculated or new leaves.

When temperatures were raised to 33 °C, some resistant plants temporarily showed mosaic and deformation symptoms — indicating that the resistance response was suppressed under heat, not permanently broken. Once temperatures returned to 24 °C, the resistance fully recovered: new leaves were clean, and the virus was again undetectable.

The study also showed that under extreme virus pressure, such as grafting resistant scions onto infected rootstocks, the virus could still move into resistant tissue. This confirms that pressure, not heat alone, is the decisive factor in whether symptoms appear.

In short: heat can temporarily weaken R-gene responses, but the resistance returns when temperatures drop — and high virus pressure is the real trigger for visible symptoms.

Conclusion

The idea that “heat breaks HREZ” oversimplifies how R-gene resistance works. HREZ remains effective under normal and moderately high temperatures, and even when extreme heat temporarily suppresses the response, cooler periods restore full function. The real challenge arises only when prolonged heat and high virus pressure occur together — a stress combination that affects almost any R-gene system.

Across warm regions worldwide, HREZ continues to perform strongly when virus pressure is managed well. Used alongside solid hygiene practices, it remains one of the most reliable tools growers have for controlling ToBRFV.