Mol. Cells 2022; 45(12): 883-885
Published online December 7, 2022
https://doi.org/10.14348/molcells.2022.0150
© The Korean Society for Molecular and Cellular Biology
Correspondence to : jl924@snu.ac.kr
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
Plants often face a wide range of biotic and extreme environmental stresses as sessile organisms. These stresses cause physiological changes, resulting in plant growth and yield penalty. Since plants lack a circulatory immune system, they solely depend on the cell-autonomous local responses, for example, the transportation of signaling molecules through a membrane-separated vesicular system (Kwon et al., 2020; Won and Kim, 2020). Elevated temperature profoundly impacts plant defense responses and render plants vulnerable to pathogens. Research breakthroughs elucidating the underlying molecular mechanisms of this pathway were made in the last decade. Zhu et al. (2010) reported that a mutation in the resistance (
Calcium signaling is essential in plant defense responses associated with PTI and ETI (Wang et al., 2009). Within the cell, calcium signals are transduced by binding calcium ions to calmodulins (CaMs), which subsequently bind to CaM binding proteins (Bouché et al., 2005). In
GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) forms GBPL defense-activated biomolecular condensates called GDACs, which bind to the promoters of
To survive in an unfavorable environment, plants must manage limited resources to relocate to the designated organ for growth and accelerate their defense mechanisms. During this process, plants often activate defense signaling at the expense of growth. However, recent studies (Figueroa-Macías et al., 2021; Neuser et al., 2019) suggested that there could be an alternative instead of this ‘trade-off’ signaling between growth and defense regulatory mechanism that reprogram developmental pathways based on the hostile environment. When Kim et al. (2022) over-expressed
Recent studies (Jing et al., 2019; Okada et al., 2021; Poncini et al., 2017) reported that root growth was impaired by perceiving biotic or abiotic stress signals. Consistent with this finding, we also identified that plant elicitor peptide 1 (PEP1), a general sensor of biotic and abiotic stresses, affects the reprograming of
In summary, the study led by Kim et al. (2022) provided comprehensive evidence of how environmental factors control the SA-induced defense signaling pathway in connection to plant immunity. The author’s results will serve as a benchmark for understanding the concept of the plant-environment-disease triangle and prompt future researchers to identify the mechanistic approach toward the underlying defense response pathways.
We thank all members of the Lee lab for their discussions and comments at various stages. This work was supported by the grants NRF-2018R1A5A1023599 and NRF-2021R1A2C3006061 to J.-Y.L. from the National Research Foundation of Korea. S.D. was supported by the Brain Korea 21 Four Program.
S.D. and J.-Y.L. wrote the paper.
The authors have no potential conflicts of interest to disclose.
Mol. Cells 2022; 45(12): 883-885
Published online December 31, 2022 https://doi.org/10.14348/molcells.2022.0150
Copyright © The Korean Society for Molecular and Cellular Biology.
Souvik Dhar1 and Ji-Young Lee1,2,3,*
1School of Biological Science, College of Natural Sciences, Seoul National University, Seoul 08826, Korea, 2Plant Genomics and Breeding Institute, Seoul National University, Seoul 08826, Korea, 3Plant Immunity Research Center, Seoul National University, Seoul 08826, Korea
Correspondence to:jl924@snu.ac.kr
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
Plants often face a wide range of biotic and extreme environmental stresses as sessile organisms. These stresses cause physiological changes, resulting in plant growth and yield penalty. Since plants lack a circulatory immune system, they solely depend on the cell-autonomous local responses, for example, the transportation of signaling molecules through a membrane-separated vesicular system (Kwon et al., 2020; Won and Kim, 2020). Elevated temperature profoundly impacts plant defense responses and render plants vulnerable to pathogens. Research breakthroughs elucidating the underlying molecular mechanisms of this pathway were made in the last decade. Zhu et al. (2010) reported that a mutation in the resistance (
Calcium signaling is essential in plant defense responses associated with PTI and ETI (Wang et al., 2009). Within the cell, calcium signals are transduced by binding calcium ions to calmodulins (CaMs), which subsequently bind to CaM binding proteins (Bouché et al., 2005). In
GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) forms GBPL defense-activated biomolecular condensates called GDACs, which bind to the promoters of
To survive in an unfavorable environment, plants must manage limited resources to relocate to the designated organ for growth and accelerate their defense mechanisms. During this process, plants often activate defense signaling at the expense of growth. However, recent studies (Figueroa-Macías et al., 2021; Neuser et al., 2019) suggested that there could be an alternative instead of this ‘trade-off’ signaling between growth and defense regulatory mechanism that reprogram developmental pathways based on the hostile environment. When Kim et al. (2022) over-expressed
Recent studies (Jing et al., 2019; Okada et al., 2021; Poncini et al., 2017) reported that root growth was impaired by perceiving biotic or abiotic stress signals. Consistent with this finding, we also identified that plant elicitor peptide 1 (PEP1), a general sensor of biotic and abiotic stresses, affects the reprograming of
In summary, the study led by Kim et al. (2022) provided comprehensive evidence of how environmental factors control the SA-induced defense signaling pathway in connection to plant immunity. The author’s results will serve as a benchmark for understanding the concept of the plant-environment-disease triangle and prompt future researchers to identify the mechanistic approach toward the underlying defense response pathways.
We thank all members of the Lee lab for their discussions and comments at various stages. This work was supported by the grants NRF-2018R1A5A1023599 and NRF-2021R1A2C3006061 to J.-Y.L. from the National Research Foundation of Korea. S.D. was supported by the Brain Korea 21 Four Program.
S.D. and J.-Y.L. wrote the paper.
The authors have no potential conflicts of interest to disclose.