Prof. Kwak, June M.
Professor, Group Leader, Institute for Basic Science;
We are interested in understanding how environmental changes cause adjustments in plant growth, senescence and death as well as the metamorphosis from cell growth to cell death. Our studies will help to predict physiological and genetic changes in plants during the plant’s lifespan that global climate change causes and also aid in preparing for the future ecological reshaping.
Global climate change is unequivocal due to the elevated concentration of greenhouse gases, and includes global warming and drought as well as fresh water scarcity. As global temperatures rise, it is predicted that we will encounter increased variability in amounts and distribution of precipitation, increased water demand, and enhanced susceptibility to drought. This will result in profound impacts on global fresh water resources, 65% of which are used for plants. All these environmental changes will influence the physiology of plants, including cell growth, senescence, and death. Understanding the molecular mechanisms underlying the plant growth and death control in response to environmental changes will enable us to predict, at least in part, how plants will modify their physiology for adaptation to global climate change, which will lead to improved strategies for developing crop plants that are more tolerant to the harsh environment.
<Plants continuously interact with everlasting changes in their environment.>
As environmental cues tremendously affect plant physiology, a vast amount of research has been focused on understanding how plants cope with various biotic and abiotic signals. In contrast, there is very limited information as to how everlasting changes in environment modulate the genetic and epigenetic mechanisms of plant lifespan and senescence. This is partly due to the fact that plant senescence is a complex genetic program that is continuously adjusted to assure plant growth and survival, thus making experimental analyses challenging. Moreover, plant aging is an integrated output of all the previous life history including interaction with environment, and its analysis requires highly reproducible growth conditions to have a reproducible senescence pattern and lifespan. Thus, use of multidisciplinary approaches, including systems-level analysis, molecular genetics, cell biology and physiology, is required to address the fundamental biological question about aging processes modulated by environmental changes, which will lead to unprecedented mechanistic understanding of the cellular networks governing plant senescence and its interaction with environment. In addition, such analyses will also provide a fundamental insight into the evolution of the aging and cell death programs of biological organisms in various ecological environments.
<Biogenesis of miRNA in plants.>
MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and various cellular responses, including plant growth and senescence. The Mediator (Med) recruits RNA polymerase II (Pol II) to promoters of microRNA genes to promote the transcription of MIR genes by bridging the interaction between the transcription factors (TF) and Pol II. MIR genes are transcribed into 5’ capped and 3’ polyadenylated pri-miRNAs. Pri-miRNAs undergo processing to give rise to small RNA duplexes containing the miRNA and the antisense miRNA by the DCL1 complex. The duplex is methylated on the 2′ OH of the 3′ terminal nucleotides by HEN1. miRNA strand is bound by AGO1 to direct mRNA cleavage or translational inhibition.
Another level of complexity is present in analyzing the genetic and epigenetic regulation of plant lifespan modulated by environmental signals. For example, when a specific environmental stimulus is given to plant cells, even the same type of cells often show different responses. One of the important puzzles in biology in general and also in plant’s response to environment is how the individual cells collectively perceive and process the environmental information. Responses monitored in heterogeneous tissues may reflect mixtures of unique responses in individual cell types. In addition, it is largely unknown how environmental cues affect plant lifespan and senescence at the cellular and the whole plant level. In order to achieve complete understanding of cellular networks governing senescence and environmental interaction, establishment of a model system for cellular senescence is pivotal, and systems analysis of a single cell or cell-type specific samples is required.
<EM image of guard cells, one of the cell-types that we are trying to understand cellular networks governing senescence and environmental interaction.>
To address these important questions, we carry out following research projects.
1. Conduct systems analysis of environmental modulation of senescence and lifespan
2. Establish a cellular model system for studying cellular aging and interaction with environmental stimuli
3. Investigate epigenetic regulation of senescence and aging in response to environmental cues
4. Conduct systems analysis of ROS and calcium signaling networks regulating plant senescence and interaction with environment
- F Villiers, O Bastien and JM Kwak (2014) R. S. WebTool, a web server for random sampling-based significance evaluation of pairwise distances. Nucleic Acids Res., 42 (W1): W198-W204.
- L Zhang, DP Foreman, PA Grant, B Shrestha, SA Moody, F Villiers, JM Kwak and A Vertes (2014) In situ metabolic analysis of single plant cells by capillary microsampling and electrospray ionization mass spectrometry with ion mobility separation. Analysist 139: 5079-5085.
- AM Jones, S Lalonde, CH Ho, M Xu, CH You, R Wang, Y Xuan, MI Sardi, S A Parsa, E Smith-Valle, G Pilot, R Pratelli, G Grossmann, BR Acharya, H-C Hu, F Villiers, K Takeda, SM Assmann, J Chen, JM Kwak, JI Schroeder, R Albert, SY Rhee and WB Frommer (2014) Border control – the membrane-based interaction of Arabidopsis. Science 344: 711-716
- C Zhang, Q Xie, R Anderson, G Ng, N Seitz, CR McClung, JM McDowell, D Kong, JM Kwak and H Lu (2013) Crosstalk between the circadian clock and innate immunity in Arabidopsis. PLoS Pathogen, 9(6): e1003370. doi:10.1371/journal.ppat.1003370
- D Cho, F Villiers, L Kroniewicz, S Lee, Y Seo, K Hirschi, N Leonhardt and JM Kwak (2012) Vacuolar CAX1 and CAX3 influence auxin transport in guard cells via regulation of apoplastic pH. Plant Physiol. 160: 1293-1302.
- F Jammes, H-C Hu, R Bouten, F Villiers and JM Kwak (2011) Plant calcium-permeable channels. FEBS J. 278: 4262-4276
- F Jammes, CJ Song, D Shin, S Munemasa, K Takeda, D Gu, D Cho, S Lee, R Giordo, S Sritubtim, N Leonhardt, EB Ellis, Y Murata and JM Kwak (2009) Two MAP kinases, MPK9 and MPK12, are preferentially expressed in guard cells and positively regulate ROS-mediated ABA signaling. Proc. Nat’l. Acad. Sci. USA, 106: 20520-20525.
- D Cho, SA Kim, Y Murata, S Lee, S-K Jae, HG Nam and JM Kwak (2009). Deregulated expression of a plant glutamate receptor homolog impairs long-term Ca2+-programmed stomatal closure. Plant J. 58: 437-449.
- JM Kwak, IC Mori, N Leonhardt, Z-M Pei, M-A Torres, J Dangl, R Bloom, S Bodde, JDG Jones and JI Schroeder (2003) NADPH oxidase AtrbohD and AtrbohF genes function in ROS-dependent ABA signaling in Arabidopsis. EMBO J., 22, 2623-2633.
- JM Kwak, J Moon, Y Murata, K Kuchitsu, N Leonhardt, A DeLong and JI Schroeder (2002) Disruption of a guard cell-expressed protein phosphatase 2A regulatory subunit, RCN1, confers abscisic acid insensitivity in Arabidopsis. Plant Cell, 14, 2849-2861.
- V Hugouvieux, JM Kwak and JI Schroeder (2001) An mRNA cap binding protein, ABH1, modulates early abscisic acid signal transduction in Arabidopsis. Cell, 106, 477-487.