Blog Myth #3: More genes is always better than one gene

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Blog Myth #3: More genes is always better than one gene

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

More genes is always better than one gene

By Manus Thoen, Sr. Researcher Phythopathology

In resistance breeding, “more genes” sounds like “more protection.” But in practice, stacking resistances isn’t automatically better. And in many cases, a single, well-chosen dominant gene delivers the strongest, cleanest, and most reliable resistance.

Single-gene resistance: the foundation of our tomato portfolio

At Enza Zaden, all major high-resistance traits in tomato — ToMV, Fol, Pf, and now HREZ — are built on single, well-characterized dominant genes. These genes are stable, predictable, and highly effective when placed in the right genetic background.

A classic example is Tm-2², the tobamovirus resistance gene used for decades across the industry. It’s a single dominant R-gene, and it remained effective for an exceptionally long time before resistance-breaking strains appeared. This remains of the clearest historical examples of true High Resistance based on a single dominant gene with tremendous value for the tomato industry.

Sergio de la Fuente van Bentem, Expert Researcher Phytopathology

“All our major tomato resistances are single-gene based. That includes HREZ, but also long-standing resistances like the Tm-22 , a dominant resistance gene working for over 50 years. This resistance gene has been regarded as a true ‘High Resistance” against ToMV across the industry, and HREZ is in my ways very similar to Tm-22.

Why single dominant genes matter in breeding

From a breeding perspective, a dominant gene is a gift:

  • easy to track
  • fast to introgr
  • clean genetics
  • reliable expression across backgrounds

Stacking multiple recessive genes, by contrast, is slow and complex. 

Some breeding programs in our industry rely on combinations of recessive genes. The mechanisms underlying these genes can contribute to partial protection and often only function in a homozygous state, meaning you need a copy of those genes from both parents. Combining these genes can help, but it is a fundamentally different breeding strategy from using a single dominant R gene.

One recessive gene alone doesn’t give enough resistance. And using it in a heterozygous state doesn’t work at all. So you will need to combine two weaker genes in that case. Not because and “more is better”, but to compensate for a shortcoming.

Nejra Solo, Molecular Marker Specialist

“Having a single dominant resistant gene really brings speed clarity to the whole breeding process.”

Looking ahead: strategic stacking, not blind pyramiding

Stacking becomes valuable when genes have different mechanisms that act on the same pathogen. That’s when they can share the load, reduce viral pressure, and protect each other’s durability.

This is where the future lies: HREZ as the core, supported by complementary mechanisms like Tm-1 when the time is right.

Lessons from COVID

When COVID‑19 emerged, the world quickly learned that not all forms of protection work in the same way. Mouth masks became a crucial tool — not because they killed the virus, but because they reduced spread. They lowered exposure, slowed transmission, and bought time. But to actually clear the virus inside the body, you needed something else entirely: an immune system trained by vaccination.

That distinction is useful when thinking about ToBRFV resistance.

Some resistance mechanisms in tomato behave a bit like masks. They don’t eliminate the virus; they reduce viral load, slow movement, or limit replication. These mechanisms can be valuable, especially when combined with good hygiene, but they are not designed to actively destroy the virus once it enters the cell.

HREZ is different

It functions more like the “vaccinated immune system” in this analogy — a true R‑gene response that recognizes the virus and triggers a hypersensitive reaction to stop it. It’s the only mechanism we know today that can actively kill infected cells and prevent systemic spread.

And just like during COVID, masks and vaccines weren’t competing tools — they were complementary. The same is true here. Mechanisms that reduce spread can support HREZ, but they are not substitutes for it. HREZ provides the strong, specific immune recognition; other mechanisms help reduce pressure. Together, they form a more resilient system.

Jeroen Rouppe van der Voort, Research Lead Expert Biotechnology

“HREZ works through a very strong and specific recognition mechanism. It’s the only way to actively kill the virus when it’s in the plant. Other known resistance mechanisms work in different ways. HREZ is the foundation of resistance. When stacking with these other mechanisms, you need the strong resistance foundation that only HREZ can offer.”

What the data shows

Public research on tobamovirus resistance shows that tomato plants use different biological mechanisms, and these mechanisms do not all offer the same level or type of protection. The best‑known example is Tm‑2², a dominant NLR‑type resistance gene that recognizes the tobamovirus movement protein and triggers a hypersensitive response (Lanfermeijer et al., 2005). This single gene protected global tomato production for decades before resistance‑breaking strains appeared, illustrating how powerful one well‑functioning dominant gene can be.

Alongside these strong R‑gene systems, researchers have also identified other forms of resistance in wild tomato species. Several accessions of Solanum habrochaites and S. peruvianum show partial resistance or tolerance to ToBRFV and related tobamoviruses, where the virus still enters the plant but accumulates more slowly or causes milder symptoms (Jewehan et al., 2022). These mechanisms reduce viral spread rather than eliminating the virus, making them biologically different from dominant R‑gene responses. Tm-1, located on chromosome 2, is another well studied tobamovirus resistance gene. Different in comparison to HREZ, as Tm-1 inhibits replication of the virus. In itself not sufficient to fully protect against ToBRFV, but it can definitely positively contribute when combined with right genetics (Zinger et al., 2025), like HREZ.

Because these mechanisms act at different points in the infection cycle, stacking only makes sense when the genes involved are complementary (Michelmore et al., 2013). In practice, this means a strong dominant R gene provides the essential recognition trigger, and additional mechanisms can help share the load, but they cannot replace the core function of an R gene.

Bottom line

More genes isn’t automatically better. The right gene — deployed cleanly and precisely — is what matters. HREZ gives us a strong, dominant, clean foundation today. And in the future, strategic stacking can help protect its durability, ensuring growers benefit from long-lasting, reliable resistance.