A breakthrough in plant defense after decades of research
How cooperation and sustained research lead to a discovery 34 years in the making
Plants have ways of defending themselves against wounding by insect pests, and a key feature of this wound response was uncovered after 34 years of collaboration and mentorship.
Chuanyou Li, a former postdoctoral researcher in Gregg Howe’s lab at the MSU-DOE Plant Research Laboratory, or PRL, has solved a mystery that goes back to Howe’s own postdoc days.
Li found the receptor for systemin, a wound signal that travels through the plant, warning that something is wrong. For example, if a caterpillar is nibbling on a tomato leaf, the plant will respond by producing defense compounds that will make the caterpillar feel sick.
This finding has implications for understanding how plants respond to threats and allows scientists to produce plants that are more resilient. In the future, it may be possible to engineer plants with optimized receptors that will allow them to ward off threats without penalty to growth.
The systemin receptor finding was published in Developmental Cell.
Beginnings
This research started in the 1990s in Clarence “Bud” Ryan’s lab at Washington State University. Ryan had identified the first peptide signal in plants, systemin.
As a graduate student at UCLA, Howe heard Ryan give a talk.
“That really piqued my interest when I was a graduate student, and I actually wrote him a letter,” said Howe who is currently an MSU Research Foundation Professor in the PRL, the Department of Biochemistry & Molecular Biology and the Plant Resilience Institute. “I wrote an old-fashioned letter and expressed interest in joining his lab as a postdoc. And it all worked out and I ended up at WSU.”
One of Howe’s projects in the Ryan lab was looking for the systemin receptor, which is a protein that binds to the peptide signal and initiates the response in the cell. If systemin is the message, the receptor is the phone which receives it.
Howe used a genetic approach in tomato to look for the receptor. He found mutant tomato plants – plants with an alteration to their DNA – that did not respond to systemin like their wild-type counterparts.
The technology wasn’t ready yet—despite knowing that the mutants were “blind” to systemin, Howe was unable to identify the putative receptor gene that was defective in the mutants. In 1997, he was offered a position at Michigan State University in the PRL as an assistant professor. Ryan let Howe take the mutants with him.
In academia, transitioning from postdoctoral fellow to faculty can be tricky – sometimes, your former mentor will not let you take a project to your new institution. Howe found Ryan to be very generous in giving him all the mutants, crediting that generosity with helping him get the position at the PRL and launching his independent research career.
Passing the torch
Howe continued to study the mutants while at the PRL, with no luck finding the receptor.
“Various students and postdocs worked on it over the years, and we were not successful finding the gene because back then, this was in the early 2000s,” Howe said. “Mapping and cloning genes was much more difficult than it is now.”
One such postdoc was Chuanyou Li, who worked in the Howe lab from 1999-2003 and is now the Dean and a professor in the College of Life Sciences at Shandong Agricultural University, China. Despite successfully cloning other genes that control the wound response during this time, including SPR2 and JL1 (ACX1), the systemin receptor eluded Li and Howe.
“Gregg passed me the spr1 mutant when I established my own lab in 2003 at the Institute of Genetics & Developmental Biology in Beijing,” Li said. He moved to Shandong in 2023. “After 20 years of hard working, we finally got success in the long-lasting battle to identify the SPR1 locus.”
Using next generation sequencing technologies, Li was able to sequence the entire genome of the mutant tomato line. This allowed the researchers to see all the genes that make up this plant and compare it to the genome of wild-type tomatoes. The data showed that the receptor was produced by two similar genes, now called systemin receptor 1, or SYR1, and SYR2.
“This study beautifully answers a long-standing question of how plants appropriately respond to on-going wounding damage without excessively sacrificing growth and has implications for uncoupling defense-growth trade-offs,” Li said.
Li collaborated with Howe on research that revealed the function of these genes.
“In this paper we finally identify the mutation at the molecular level,” Howe said. “The exciting thing was indeed, as we had hoped back then, it is a mutation that abolishes the function of the systemin receptor.”
Generational Knowledge
These achievements could not have happened without generations of scientists training and supporting one another.
“Gregg is a wonderful mentor for postdocs and students, whose dedication and enthusiasm for science are contagious,” Li said. “He is able to create a stimulating research environment in which postdocs and students could thrive in the ‘hot’ research fields of systemin and jasmonate.”
Seeing the success of a former mentee is a rewarding experience for any teacher.
“Whenever someone identifies a receptor in plant biology, we put that at the pinnacle,” Howe said. “Chuanyou picked this up many years later, knowing the technology had advanced to the point where he could maybe solve the problem. It's very gratifying from my perspective to see him pick this old project up and finally answer the question.”
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