BnaA07.SUC2 regulated by BnaA05.MYC2 in jasmonate pathway promotes oilseed rape susceptibility to Plasmodiophora brassicae.
Liu J, Xu Z, Li Y, Wu S, Ni Z
Crispr
Clubroot destroys canola and cabbage crops worldwide, and this discovery points to a specific genetic switch that could be edited to protect the broccoli, kale, and cabbage in your garden from one of their worst enemies.
A destructive soil pathogen called clubroot hijacks a protein in canola roots that normally moves sugar around the plant, essentially turning the plant into a buffet for the invader. Scientists found that a natural plant defense hormone initially tries to block this sugar transporter, but the pathogen eventually wins by suppressing that defense. When researchers used gene editing to permanently disable the transporter, the plants became much harder for clubroot to infect.
Key Findings
CRISPR/Cas9 knockout of the BnaA07.SUC2 sucrose transporter gene significantly enhanced clubroot resistance in oilseed rape, while overexpression increased disease susceptibility.
The transcription factor BnaA05.MYC2, activated by jasmonate defense signaling, directly represses BnaA07.SUC2 expression — but this repression is overridden as infection progresses and the pathogen suppresses jasmonate signaling.
Functional complementation experiments confirmed BnaA07.SUC2 is the key susceptibility factor: restoring it in resistant backgrounds re-established full susceptibility to Plasmodiophora brassicae.
chevron_right Technical Summary
Researchers discovered that a sugar-transporting protein in oilseed rape (canola) acts as a gateway that lets a devastating root pathogen steal nutrients from the plant. By identifying and disabling this transporter using gene editing, they were able to make plants significantly more resistant to clubroot disease.
Abstract Preview
Biotrophic pathogens depend on host carbon sources for proliferation. Here, we identified BnaA07.SUC2 in oilseed rape (Brassica napus cv. Westar), which encodes a plasma membrane-localized proton-d...
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