Biomedical subjects

Pyung Ok Lim

Publications and source records attributed to Pyung Ok Lim.

8 recordsLinked to original sources

PubMed2007

Leaf senescence.

Leaf senescence constitutes the final stage of leaf development and is critical for plants' fitness as nutrient relocation from leaves to reproducing seeds is achieved through this process. Leaf senescence involves a coordinated action at the cellular, tissue, organ, and organism levels under the control of a highly regulated genetic program. Major breakthroughs in the molecular understanding of leaf senescence were achieved through characterization of various senescence mutants and senescence-associated genes, which revealed the nature of regulatory factors and a highly complex molecular regulatory network underlying leaf senescence. The genetically identified regulatory factors include transcription regulators, receptors and signaling components for hormones and stress responses, and regulators of metabolism. Key issues still need to be elucidated, including cellular-level analysis of senescence-associated cell death, the mechanism of coordination among cellular-, organ-, and organism-level senescence, the integration mechanism of various senescence-affecting signals, and the nature and control of leaf age.

Apoptosis↗

PubMed2006

Cytokinin-mediated control of leaf longevity by AHK3 through phosphorylation of ARR2 in Arabidopsis.

Cytokinins are plant hormones with profound roles in growth and development, including control of leaf longevity. Although the cytokinin signal is known to be perceived by histidine kinase receptors, the underlying molecular mechanism and specificity of the receptors leading to delayed leaf senescence have not yet been elucidated. Here, we found that AHK3, one of the three cytokinin receptors in Arabidopsis, plays a major role in controlling cytokinin-mediated leaf longevity through a specific phosphorylation of a response regulator, ARR2. This result was obtained through identification of a gain-of-function Arabidopsis mutant that shows delayed leaf senescence because of a missense mutation in the extracellular domain of AHK3. A loss-of-function mutation in AHK3, but not of the other cytokinin receptors, conferred a reduced sensitivity to cytokinin in cytokinin-dependent delay of leaf senescence and abolished cytokinin-dependent phosphorylation of ARR2. Consistently, transgenic overexpression of wild-type, but not an unphosphorylatable mutant ARR2, led to delayed senescence of leaves.

Aging↗

PubMed2005

Phytochrome-specific type 5 phosphatase controls light signal flux by enhancing phytochrome stability and affinity for a signal transducer.

Environmental light information such as quality, intensity, and duration in red (approximately 660 nm) and far-red (approximately 730 nm) wavelengths is perceived by phytochrome photoreceptors in plants, critically influencing almost all developmental strategies from germination to flowering. Phytochromes interconvert between red light-absorbing Pr and biologically functional far-red light-absorbing Pfr forms. To ensure optimal photoresponses in plants, the flux of light signal from Pfr-phytochromes should be tightly controlled. Phytochromes are phosphorylated at specific serine residues. We found that a type 5 protein phosphatase (PAPP5) specifically dephosphorylates biologically active Pfr-phytochromes and enhances phytochrome-mediated photoresponses. Depending on the specific serine residues dephosphorylated by PAPP5, phytochrome stability and affinity for a downstream signal transducer, NDPK2, were enhanced. Thus, phytochrome photoreceptors have developed an elaborate biochemical tuning mechanism for modulating the flux of light signal, employing variable phosphorylation states controlled by phosphorylation and PAPP5-mediated dephosphorylation as a mean to control phytochrome stability and affinity for downstream transducers.

Arabidopsis↗

PubMed2005

The molecular and genetic control of leaf senescence and longevity in Arabidopsis.

The life of a leaf initiated from a leaf primordium ends with senescence, the final step of leaf development. Leaf senescence is a developmentally programmed degeneration process that is controlled by multiple developmental and environmental signals. It is a highly regulated and complex process that involves orderly, sequential changes in cellular physiology, biochemistry, and gene expression. Elucidating molecular mechanisms underlying such a complex, yet delicate process of leaf senescence is a challenging and important biological task. For the past decade, impressive progress has been achieved on the molecular processes of leaf senescence through identification of genes that show enhanced expression during senescence. In addition, Arabidopsis has been established as a model plant for genetic analysis of leaf senescence. The progress on the characterization of genetic mutants of leaf senescence in Arabidopsis has firmly shown that leaf senescence is a genetically controlled developmental phenomenon involving numerous regulatory elements. Especially, employment of global expression analysis as well as genomic resources in Arabidopsis has been very fruitful in revealing the molecular genetic nature and mechanisms underlying leaf senescence. This progress, including molecular characterization of some of the genetic regulatory elements, are revealing that senescence is composed of a complex regulatory network. In this review, we will present current understanding of the molecular genetic mechanisms by which leaf senescence is regulated and processed, focusing mostly on the regulatory factors of senescence in Arabidopsis. We also present a potential biotechnological implication of leaf senescence studies on the improvement of important agronomic traits such as crop yield and post-harvest shelf life. We further provide future research prospects to better understand the complex regulatory network of senescence.

Aging↗

PubMed2005

Comparative transcriptome analysis reveals significant differences in gene expression and signalling pathways between developmental and dark/starvation-induced senescence in Arabidopsis.

An analysis of changes in global gene expression patterns during developmental leaf senescence in Arabidopsis has identified more than 800 genes that show a reproducible increase in transcript abundance. This extensive change illustrates the dramatic alterations in cell metabolism that underpin the developmental transition from a photosynthetically active leaf to a senescing organ which functions as a source of mobilizable nutrients. Comparison of changes in gene expression patterns during natural leaf senescence with those identified, when senescence is artificially induced in leaves induced to senesce by darkness or during sucrose starvation-induced senescence in cell suspension cultures, has shown not only similarities but also considerable differences. The data suggest that alternative pathways for essential metabolic processes such as nitrogen mobilization are used in different senescent systems. Gene expression patterns in the senescent cell suspension cultures are more similar to those for dark-induced senescence and this may be a consequence of sugar starvation in both tissues. Gene expression analysis in senescing leaves of plant lines defective in signalling pathways involving salicylic acid (SA), jasmonic acid (JA) and ethylene has shown that these three pathways are all required for expression of many genes during developmental senescence. The JA/ethylene pathways also appear to operate in regulating gene expression in dark-induced and cell suspension senescence whereas the SA pathway is not involved. The importance of the SA pathway in the senescence process is illustrated by the discovery that developmental leaf senescence, but not dark-induced senescence, is delayed in plants defective in the SA pathway.

Arabidopsis↗

PubMed2004

The delayed leaf senescence mutants of Arabidopsis, ore1, ore3, and ore9 are tolerant to oxidative stress.

Reactive oxygen species play a critical role in mediating the oxidative damage that causes senescence in a variety of aerobic organisms, from yeast to mammals. Genetic studies of these organisms have revealed that extended longevity is frequently associated with an increased resistance to stress. However, the relationship between life span and oxidative stress tolerance in plants is poorly understood. We have investigated the responses to oxidative stress in the delayed leaf senescence mutants of Arabidopsis thaliana, ore1, ore3, and ore9. The detached leaves of these mutants exhibit increased tolerance to various types of oxidative stress. The ore1, ore3, and ore9 mutants were also more tolerant to oxidative stress at the level of the whole plant, as determined by measuring physiological and molecular changes associated with oxidative stress. However, the activities of antioxidant enzymes were similar or lower in the mutants, as compared to wild type. These results suggest that the increased resistance to oxidative stress in the ore1, ore3, and ore9 mutants is not due to enhanced activities of these antioxidant enzymes. Taken together, our findings provide genetic evidence that oxidative stress tolerance is linked to control of leaf longevity in plants.

Arabidopsis↗

PubMed2003

Molecular genetics of leaf senescence in Arabidopsis.

Leaf senescence is a developmentally programmed degeneration process that constitutes the final step of leaf development and is controlled by multiple developmental and environmental signals. In addition to the information obtained from other plants, Arabidopsis has, as a model system, contributed to our understanding of this complex phenomenon in molecular genetic terms. Recent discoveries have identified several genetic mutants and potential regulatory components in Arabidopsis. Identifying further mutants that exploit novel biological resources, screening Scheme and a global functional analysis of senescence-associated genes in Arabidopsis should increase our understanding of the complex regulatory networks.

Aging↗

PubMed2003

The Arabidopsis COG1 gene encodes a Dof domain transcription factor and negatively regulates phytochrome signaling.

Light is a critical environmental factor that influences almost all developmental aspects of plants, including seed germination, seedling morphogenesis, and transition to reproductive growth. Plants have therefore developed an intricate network of mechanisms to perceive and process environmental light information. To further characterize the molecular basis of light-signaling processes in plants, we screened an activation tagging pool of Arabidopsis for altered photoresponses. A dominant mutation, cog1-D, attenuated various red (R) and far-red (FR) light-dependent photoresponses. The mutation was caused by overexpression of a gene encoding a member of the Dof family of transcription factors. The photoresponses in Arabidopsis were inversely correlated with the expression levels of COG1 mRNA. When the COG1 gene was overexpressed in transgenic plants, the plants exhibited hyposensitive responses to R and FR light in a manner inversely dependent on COG1 mRNA levels. On the other hand, transgenic lines expressing antisense COG1 were hypersensitive to R and FR light. Expression of the COG1 gene is light inducible and requires phytochrome A (phyA) for FR light-induced expression and phytochrome B (phyB) for R light-induced expression. Thus, the COG1 gene functions as a negative regulator in both the phyA- and phyB-signaling pathways. We suggest that these phytochromes positively regulate the expression of COG1, a negative regulator, as a mechanism for fine tuning the light-signaling pathway.

Amino Acid Sequence↗