91porn

Sept. 16, 2025

By Christian Danve M. Castroverde, Associate Professor, Biology

The global COVID-19 pandemic in 2020 spurred a time-sensitive race to develop next-generation vaccines. Effective against numerous diseases, vaccines are important in training our immune systems to remember infectious agents. Vaccines allow mobile immune cells that patrol our body to produce antibodies, which are used to remember and subsequently neutralize future infections.

Unlike humans, plants do not possess these specialized, mobile immune cells that produce antibodies. Instead, plants depend on a different form of immune memory called systemic acquired resistance (SAR). A localized infection in a leaf, for example, primes distant, uninfected plant tissues for increased defences against future pathogenic attack.

In a way, one could consider SAR as plant “vaccination.” But instead of antibodies, SAR is underpinned by a cascade of important signals, which include the immune-activating molecule called N-hydroxypipecolic acid (NHP). NHP is derived from the essential amino acid lysine, which is converted into pipecolic acid (Pip) by the enzymes ALD1 and SARD4. Another enzyme called FMO1 finally converts Pip into NHP, which can then boost other immune signals, like the plant defence hormone called salicylic acid that we also study in my research lab.

In our published in The Plant Journal, we discovered a disturbing trend: elevated temperatures associated with climate change sabotage the effectiveness of SAR. My former MSc student Alyssa Shields found that prior infection can prepare plants against future infection at ambient temperatures, but this immune preparedness is lost under warmer conditions.

Together with our collaborator Lingya Yao, we found the culprit to be the loss of NHP production. This was a general trend in all plants we studied, like the model species Arabidopsis thaliana, as well as important agricultural crops like tomato and canola. The loss of NHP production was due to NHP biosynthetic genes – including ALD1 and FMO1 – being switched off at warm temperatures.

But here is an important twist: when we supplied NHP or Pip externally to the plant, it was able to restore its immune preparedness against subsequent pathogenic attack even at elevated temperatures. This provides important evidence that the failure of plant systemic immunity under climate warming is primarily due to the lack of NHP.

Genetically, we found the main cause to be the transcription factors CBP60g and SARD1, which act as master switches that can turn on or turn off NHP genes, such as ALD1 and FMO1. As it turns out, heat suppresses the levels of CBP60g and SARD1, leading to a domino effect of abolished NHP (and therefore, SAR) at higher temperatures. Remarkably, engineering plants that have CBP60g or SARD1 always turned on made the plant’s immune system more resilient to temperature changes.

Because of climate change, our study has major implications. Plants losing their immune memory under heat stress means decreased preparedness against infectious pathogens and resulting plant disease epidemics, which would increase vulnerabilities in agricultural and natural ecosystems. Imagine if heat eroded our own ability to remember previous infections and vaccinations – that would be a disturbing and worrying thought. In plants, that is their reality. Therefore, we need to find ways to mitigate this existential threat.

It is not all doom and gloom, however. Apart from identifying plant immune vulnerabilities, our research also offers an important roadmap for plant resilience so that they can beat the heat! Our discovery of NHP-mediated immune resilience opens avenues for current and future efforts toward bioengineering climate-smart plants. The goal is that these plants not only survive but actually resist diseases on our warming planet.

author list: Alyssa Shields, Lingya Yao, Christina Rossi, Paula Collado Cordon, Jong Hum Kim, Wasan Mudher Abu AlTemen, Sha Li, Eric Marchetta, Vanessa Shivnauth, Tao Chen, Sheng Yang He, Xiu-Fang Xin, Christian Danve M. Castroverde