Center for Plant Biology
Center for Plant Biology
News Article | August 8, 2017
Plant architecture is partly controlled through the production and perception of plant hormones. The loss of either the brassinosteroid or gibberellin plant hormones results in dwarfed plants. Removing both can increase this effect, which suggested that they control plant growth separately. That's important for scientists who want to understand how plants modify their architecture to compete for resources or create higher-yielding crops, like corn. Creating dwarf varieties of the crop plant could increase yield or keep yield steady while reducing the required inputs such as fertilizers and water. Dwarf varieties of rice and wheat were made by essentially inhibiting the response to some hormones. But in corn, the interplay among hormones makes this more complicated. Brassinosteroids and gibberellins are involved in more characteristics than just plant height in maize. Brassinosteroids, for example, are required for the tassels to contain flowers that produce pollen, and gibberellins are required for ears to only produce ovules. "Plant cells use these hormones to communicate with each other to control development in a coordinated manner. These processes determine form and execute the correct cellular programs at the correct times," said Brian Dilkes, an associate professor of biochemistry. "We will not be able to manipulate crop architecture for a particular goal if we don't understand how moving one part causes another part to change. These are highly interactive systems, and the different cellular circuits impinge on one another." In a previous study, Dilkes and collaborators investigated the genetic interactions between the genes that encode proteins that help synthesize these two hormones in maize. Maize mutants that lacked either brassinosteroids or gibberellins were interbred. Combining these mutants masked some of the physical characteristics of the parent mutants, demonstrating that the two hormones were mutually dependent in the control of branching and tassel development. In the journal Plant Direct, the Dilkes lab describes a test of these hormone interactions. By using plant growth regulators, commonly used in the horticulture industry to block production of these plant hormones, the interactions between the two hormones were tested again in maize. This work confirmed that in different parts of maize plants, the interplay between these hormones was different, demonstrating that hormone signaling is more complex than once thought. For example, maize mutants lacking gibberellin have excess branches. Using a biosynthetic inhibitor in that mutant to block brassinosteroid production eliminated that branching. So, brassinosteroids were required for the lack of gibberellin to cause branching. Dilkes said the findings show that the plant mechanisms responsible for sensing these hormones and creating physical characteristics are intertwined in ways that will take much more work to unravel. The work also showed the efficacy of using biosynthetic inhibitors to study genetic interactions in plant hormones. "Creating mutants and crossing them can take a significant amount of time and would need to be done for each species separately," Dilkes said. "Knowing that these chemicals can give us the same information will allow us to explore the interplay of these hormones in multiple species." Guri Johal, a Purdue professor of botany and plant pathology, and Norman Best, who recently completed his doctorate in the Department of Horticulture and Landscape Architecture at Purdue, were co-authors. Their paper was the first manuscript published in Plant Direct, a new, open-access journal from the American Society of Plant Biologists and the Society for Experimental Biology that will accelerate the publication of scientific discoveries in plants. It is also one of the first papers published by the Purdue Center for Plant Biology, an interdepartmental alliance of faculty working on plant biology. Next, Dilkes plans to investigate the interactions between the genes that perceive these hormones and are responsible for turning the signals into adaptive growth responses. "It is one thing to identify that these pathways interact, and something else to determine and control how that interaction takes place," he said. Best will continue to work on hormone signal integration in his new job as a postdoctoral researcher at the University of Missouri. Explore further: Revealed: New step in plant mastermind hormone's pathway More information: Norman B. Best et al. Phytohormone inhibitor treatments phenocopy brassinosteroid-gibberellin dwarf mutant interactions in maize, Plant Direct (2017). DOI: 10.1002/pld3.9
Li M.,Peking University |
Li M.,CAS Institute of Genetics and Developmental Biology |
Ma X.,Center for Plant Biology |
Chiang Y.-H.,University of California at Davis |
And 12 more authors.
Cell Host and Microbe | Year: 2014
The cyclophilin ROC1 negatively regulates immunity specified by the NLRs RPM1 and RPS2The ROC1 prolyl-peptidyl isomerase activity is required for immune response regulationROC1 catalyzes cis/trans isomerization of the RPM1-interacting protein RIN4 at Pro149Conformation surrounding RIN4 Pro149 is a molecular switch for RPM1 activation © 2014 Elsevier Inc.
PubMed | CAS Institute of Genetics and Developmental Biology, Center for Plant Biology, Peking University and University of California at Davis
Type: Journal Article | Journal: Cell host & microbe | Year: 2014
In the absence of pathogen infection, plant effector-triggered immune (ETI) receptors are maintained in a preactivation state by intermolecular interactions with other host proteins. Pathogen effector-induced alterations activate the receptor. In Arabidopsis, the ETI receptor RPM1 is activated via bacterial effector AvrB-induced phosphorylation of the RPM1-interacting protein RIN4 at Threonine 166. We find that RIN4 also interacts with the prolyl-peptidyl isomerase (PPIase) ROC1, which is reduced upon RIN4 Thr166 phosphorylation. ROC1 suppresses RPM1 immunity in a PPIase-dependent manner. Consistent with this, RIN4 Pro149 undergoes cis/trans isomerization in the presence of ROC1. While the RIN4(P149V) mutation abolishes RPM1 resistance, the deletion of Pro149 leads to RPM1 activation in the absence of RIN4 phosphorylation. These results support a model in which RPM1 directly senses conformational changes in RIN4 surrounding Pro149 that is controlled by ROC1. RIN4 Thr166 phosphorylation indirectly regulates RPM1 resistance by modulating the ROC1-mediated RIN4 isomerization.
Wang Y.,Center for Plant Biology |
Wang Y.,Tsinghua University |
Zheng X.,Center for Plant Biology |
Zheng X.,Tsinghua University |
And 13 more authors.
Autophagy | Year: 2015
Microtubules, the major components of cytoskeleton, are involved in various fundamental biological processes in plants. Recent studies in mammalian cells have revealed the importance of microtubule cytoskeleton in autophagy. However, little is known about the roles of microtubules in plant autophagy. Here, we found that ATG6 interacts with TUB8/b-tubulin 8 and colocalizes with microtubules in Nicotiana benthamiana. Disruption of microtubules by either silencing of tubulin genes or treatment with microtubule-depolymerizing agents in N. benthamiana reduces autophagosome formation during upregulation of nocturnal or oxidation-induced macroautophagy. Furthermore, a blockage of leaf starch degradation occurred in microtubule-disrupted cells and triggered a distinct ATG6-, ATG5- and ATG7-independent autophagic pathway termed starch excess-associated chloroplast autophagy (SEX chlorophagy) for clearance of dysfunctional chloroplasts. Our findings reveal that an intact microtubule network is important for efficient macroautophagy and leaf starch degradation. © 2015, Yan Wang, Xiyin Zheng, Bingjie Yu, Shaojie Han, Jiangbo Guo, Haiping Tang, Alice Yunzi L Yu, Haiteng Deng, Yiguo Hong, and Yule Liu.
Jiang S.-C.,Center for Plant Biology |
Mei C.,Center for Plant Biology |
Wang X.-F.,Center for Plant Biology |
Zhang D.-P.,Center for Plant Biology
Plant Signaling and Behavior | Year: 2014
SOAR1 is a cytosol-nucleus dual-localized pentatricopeptide repeat (PPR) protein, which we indentified recently as a crucial regulator in the CHLH/ABAR (Mg-chelatase H subunit /putative ABA receptor)-mediated signaling pathway, acting downstream of CHLH/ABAR and upstream of a nuclear ABA-responsive bZIP transcription factor ABI5. Downregulation and upregulation of SOAR1 expression alter dramatically both ABA sensitivity and expression of a subset of key, nuclear ABA-responsive genes, suggesting that SOAR1 is a hub for ABA signaling to the nucleus, and CHLH/ABAR mediates a central signaling pathway to regulate downstream gene expression through SOAR1. © Shang-Chuan Jiang, Chao Mei, Xiao-Fang Wang, and Da-Peng Zhang.