• 한국토양비료학회지
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• 제48권5호
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• pp.397-403
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• 2015

Heavy metals reduce the photosynthetic efficiency and disrupt metabolic reactions in a concentration-dependent manner. Moreover, by replacing the metal ions in metalloproteins that use essential metal ions, such as Cu, Zn, Mn, and Fe, as co-factors, heavy metals ultimately lead to the formation of reactive oxygen species (ROS). These, in turn, cause destruction of the cell membrane through lipid peroxidation, and eventually cause the plant to necrosis. Given the aforementioned factors, this study was aimed to understand the physiological responses of rice to cadmium (Cd) and arsenic (As) toxicity and the effect of essential metal ions on homeostasis. In order to confirm the level of physiological inhibition caused by heavy metal toxicity, hydroponically grown rice (Oryza sativa L. cv. Dongjin) plants were exposed with $0-50{\mu}M$ cadmium (Cd, $CdCl_2$) and arsenic (As, $NaAsO_2$) at 3-leaf stage, and then investigated malondialdehyde (MDA) contents after 7 days of the treatment. With increasing concentrations of Cd and As, the MDA content in leaf blade and root increased with a consistent trend. At 14 days after treatment with $30{\mu}M$ Cd and As, plant height showed no significant difference between Cd and As, with an identical reduction. However, As caused a greater decline than Cd for shoot fresh weight, dry weight, and water content. The largest amounts of Cd and As were found in the roots and also observed a large amount of transport to the leaf sheath. Interestingly, in terms of Cd transfer to the shoot parts of the plant, it was only transported to upper leaf blades, and we did not detect any Cd in lower leaf blades. However, As was transferred to a greater level in lower leaf blades than in upper leaf blades. In the roots, Cd inhibited Zn absorption, while As inhibited Cu uptake. Furthermore, in the leaf sheath, while Cd and As treatments caused no change in Cu homeostasis, they had an antagonist effect on the absorption of Zn. Finally, in both upper and lower leaf blades, Cd and As toxicity was found to inhibit absorption of both Cu and Zn. Based on these results, it would be considered that heavy metal toxicity causes an increase in lipid peroxidation. This, in turn, leads to damage to the conductive tissue connecting the roots, leaf sheath, and leaf blades, which results in a reduction in water content and causes several physiological alterations. Furthermore, by disrupting homeostasis of the essential metal ions, Cu and Zn, this causes complete heavy metal toxicity.

• 대한간호
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• 제26권2호통권140호
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• pp.7-14
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• 1987

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2007년도 International Meeting of the Microbiological Society of Korea
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• pp.114-116
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• 2007

• Molecules and Cells
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• 제43권10호
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• pp.841-847
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• 2020

Histone acetylation and deacetylation play central roles in the regulation of chromatin structure and transcription by RNA polymerase II (RNA Pol II). Although Hda1 histone deacetylase complex (Hda1C) is known to selectively deacetylate histone H3 and H2B to repress transcription, previous studies have suggested its potential roles in histone H4 deacetylation. Recently, we have shown that Hda1C has two distinct functions in histone deacetylation and transcription. Histone H4-specific deacetylation at highly transcribed genes negatively regulates RNA Pol II elongation and H3 deacetylation at inactive genes fine-tunes the kinetics of gene induction upon environmental changes. Here, we review the recent understandings of transcriptional regulation via histone deacetylation by Hda1C. In addition, we discuss the potential mechanisms for histone substrate switching by Hda1C, depending on transcriptional frequency and activity.

• BMB Reports
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• 제50권2호
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• pp.71-78
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• 2017

The Hippo signaling pathway plays an essential role in adult-tissue homeostasis and organ-size control. In Drosophila and vertebrates, it consists of a highly conserved kinase cascade, which involves MST and Lats that negatively regulate the activity of the downstream transcription coactivators, YAP and TAZ. By interacting with TEADs and other transcription factors, they mediate both proliferative and antiapoptotic gene expression and thus regulate tissue repair and regeneration. Dysregulation or mutation of the Hippo pathway is linked to tumorigenesis and cancer development. Recent studies have uncovered multiple upstream inputs, including cell density, mechanical stress, G-protein-coupled receptor (GPCR) signaling, and nutrients, that modulate Hippo pathway activity. This review focuses on the role of the Hippo pathway as effector of these biophysical cues and its potential implications in tissue homeostasis and cancer.

• 한국환경성돌연변이발암원학회지
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• 제23권4호
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• pp.115-130
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• 2003

Idiopathic Parkinson's disease (IPD) represents a common neurodegenerative disorder. While epidemiological studies have suggested a number of risk factors including age, gender, race, and inherited disorder, the cumulative evidence supports the view that environmental or occupational exposure to certain chemicals may contribute to the initiation and progress of Parkinsonism. More recently, clinical and laboratory investigations have led to the theory that dysregulation of iron, an essential metal to body function, may underlie IPD by initiating free radical reaction, diminishing the mitochondrial energy production, and provoking the oxidative cytotoxicity. The participation of iron in neuronal cell death is especially intriguing in that iron acquisition and regulation in brain are highly conservative and thus vulnerable to interference from other metals that bear the similar chemical reactivity. Manganese neurotoxicity, induced possibly by altering iron homeostasis, is such an example. In fact, the current interest in manganese neurotoxicology stems from two primary concerns: its clinical symptoms that resemble Parkinson's disease and its increased use as an antiknock agent to replace lead in gasoline. This article will commence with addressing the current understanding of iron-associated neurodegenerative damage. The major focus will then be devoted to the mechanism whereby manganese alters iron homeostasis in brain.

• Molecules and Cells
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• 제41권1호
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• pp.45-49
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• 2018

Autophagy is a lysosome-dependent degradation process that is essential for maintaining cellular homeostasis. In recent years, more studies have focused on the late stages of autophagy. Our group discovered and studied the terminal step of autophagy, namely autophagic lysosome reformation (ALR). ALR is the process that regenerates functional lysosomes from autolysosomes, thus maintaining lysosome homeostasis. ALR involves clathrin-mediated membrane budding from autolysosomes, elongation of membrane tubules along microtubules with the pulling force provided by the motor protein KIF5B, proto-lysosome scission by dynamin 2, and finally maturation of proto-lysosomes to functional lysosomes. In this review, we will summarize progress in unveiling the molecular mechanisms underlying ALR and its potential pathophysiological roles.

• BMB Reports
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• 제49권8호
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• pp.403-404
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• 2016

The Wnt/β-catenin signaling is an evolutionarily conserved pathway that plays a pivotal role in embryonic development and adult homeostasis. However, we have limited information about the involvement of Wnt/β-catenin signaling in the lymphatic vascular system that regulates fluid homeostasis by absorbing interstitial fluid and returning it to blood circulation. In this recent publication we report that canonical Wnt/β-catenin signaling is highly active and critical for the formation of lymphovenus valves (LVVs) and lymphatic valves (LVs). β-catenin directly associates with the regulatory elements of the lymphedema-associated transcription factor, FOXC2 and activates its expression in an oscillatory shear stress (OSS)-dependent manner. The phenotype of β-catenin null embryos was rescued by FOXC2 overexpression. These results suggest that Wnt/β-catenin signaling is a mechanotransducer that links fluid force with lymphatic vascular development.

• Molecules and Cells
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• 제43권4호
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• pp.323-330
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• 2020

Epigenetic events like DNA methylation and histone modification can alter heritable phenotypes. Zinc is required for the activity of various epigenetic enzymes, such as DNA methyltransferases (DNMTs), histone acetyltransferases (HATs), histone deacetylases (HDACs), and histone demethylases, which possess several zinc binding sites. Thus, the dysregulation of zinc homeostasis can lead to epigenetic alterations. Zinc homeostasis is regulated by Zinc Transporters (ZnTs), Zrt- and Irt-like proteins (ZIPs), and the zinc storage protein metallothionein (MT). Recent advances revealed that ZIPs modulate epigenetics. ZIP10 deficiency was found to result in reduced HATs, confirming its involvement in histone acetylation for rigid skin barrier formation. ZIP13 deficiency, which is associated with Spondylocheirodysplastic Ehlers-Danlos syndrome (SCD-EDS), increases DNMT activity, leading to dysgenesis of dermis via improper gene expressions. However, the precise molecular mechanisms remain to be elucidated. Future molecular studies investigating the involvement of zinc and its transporters in epigenetics are warranted.

• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3561-3568
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• 2012

The calcium sensing receptor (CaSR) is a member of the largest family of cell surface receptors, the G protein-coupled receptors involved in calcium homeostasis. The role of the CaSR in neoplasia appears to be homeostatic; loss of normal CaSR-induced response to extracellular calcium is observed in cancers of the colon and ovary, while increased release of PTHrP is observed in cancers of the breast, prostate and Leydig cells. Currently CaSR can be considered as a molecule that can either promote or prevent tumor growth depending on the type of cancer. Therefore, recognition of the multifaceted role of CaSR in gliomas and other malignant tumors in general is fundamental to elucidating the mechanisms of tumor progression and the development of novel therapeutic agents. Emphasis should be placed on development of drug-targeting methods to modulate CaSR activity in cancer cells.