• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2018년도 추계학술대회
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• pp.73-73
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• 2018

Bacterial leaf blight(BLB), caused by X. oryzae pv. oryzae(Xoo), is one of the most destructive diseases of rice due to its high epidemic potential. Understanding BLB resistance at a genetic level is important to further improve the rice breeding that provides one of the best approaches to control BLB disease. In the present investigation, a collection of 192 accessions was used in the genome-wide association study (GWAS) for BLB resistance loci against four Korean races of Xoo that were represented by the prevailing BLB isolates under Xoo differential system. A total of 192 accessions of rice germplasm were selected on the basis of the bioassay using four isolated races of Xoo such as K1, K2, K3 and K3a. The selected accessions was used to prepare 384-plex genotyping by sequencing (GBS) libraries and Illumina HiSeq 2000 paired- end read was used for GBS sequencing. GWAS was conducted using T ASSEL 5.0. The T ASSEL program uses a mixed linear model (MLM). T he results of the bioassay using a selected set of 192 accessions showed that a large number of accessions (93.75%) were resistant to K1 race, while the least number of accessions (34.37%) resisted K3a race. For races K2 and K3, the resistant germplasm proportion remained between 66.67 to 70.83%. T he genotypic data produced SNP matrix for a total of 293,379 SNPs. After imputation the missing data was removed, which exhibited 34,724 SNPs for association analysis. GWAS results showed strong signals of association at a threshold of [-log10(P-value)] more than5 (K1 and K2) and more than4 (K3 and K3a) for nine of the 39 SNPs, which are plausible candidate loci of resistance genes. T hese SNP loci were positioned on rice chromosome 2, 9, and 11 for K1 and K2 races, whereas on chromosome 4, 6, 11, and 12 for K3 and K3a races. The significant loci detected have also been illustrated, NBS-LRR type disease resistance protein, SNARE domain containing protein, Histone deacetylase 19, NADP-dependent oxidoreductase, and other expressed and unknown proteins. Our results provide a better understanding of the distribution of genetic variation of BLB resistance to Korean pathogen races and breeding of resistant rice.

• The Korean Journal of Physiology and Pharmacology
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• 제22권6호
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• pp.607-616
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• 2018

The effect of melatonin on juveniles with cardio fibrosis is poorly understood. We investigated whether HDACs participate in the anti-fibrotic processes regulated by melatonin during hypertrophic remodeling. Abdominal aortic constriction (AAC) was employed in juvenile rats resulting in pressure overload-induced ventricular hypertrophy and melatonin was subsequently decreased via continuous light exposure for 5 weeks after surgery. AAC rats displayed an increased cross-sectional area of myocardial fibers and significantly elevated collagen deposition compared to sham-operated rats, as measured by HE and Masson Trichrome staining. Continuous light exposure following surgery exacerbated the increase in the cross-sectional area of myocardial fibers. The expression of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 genes were all significantly enhanced in AAC rats with light exposure relative to the other rats. Moreover, the protein level of $TNF-{\alpha}$ was also upregulated in the AAC light exposure groups when compared with the sham. However, Smad4 protein expression was unchanged in the juveniles' hearts. In contrast, beginning 5 weeks after the operation, the AAC rats were treated with melatonin (10 mg/kg, intraperitoneal injection every evening) or vehicle 4 weeks, and sham rats were given vehicle. The changes in the histological measures of cardio fibrosis and the gene expressions of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 were attenuated by melatonin administration. The results reveal that melatonin plays a role in the development of cardio fibrosis and the expression of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 in cardiomyocytes.

• Asian Pacific Journal of Cancer Prevention
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• 제15권18호
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• pp.7849-7855
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• 2014

Purpose: To investigate the effect of deacetylase inhibitory trichostatin A (TSA) on anti HepG2 liver carcinoma cells and explore the underlying mechanisms. Materials and Methods: HepG2 cells exposed to different concentrations of TSA for 24, 48, or 72h were examined for cell growth inhibition using CCK8, changes in cell cycle distribution with flow cytometry, cell apoptosis with annexin V-FTIC/PI double staining, and cell morphology changes under an inverted microscope. Expression of ${\beta}$-catenin, HDAC1, HDAC3, H3K9, CyclinD1 and Bax proteins was tested by Western blotting. Gene expression for ${\beta}$-catenin, HDAC1and HDAC3 was tested by q-PCR. ${\beta}$-catenin and H3K9 proteins were also tested by immunofluorescence. Activity of Renilla luciferase (pTCF/LEF-luc) was assessed using the Luciferase Reporter Assay system reagent. The activity of total HDACs was detected with a HDACs colorimetric kit. Results: Exposure to TSA caused significant dose-and time-dependent inhibition of HepG2 cell proliferation (p<0.05) and resulted in increased cell percentages in G0/G1 and G2/M phases and decrease in the S phase. The apoptotic index in the control group was $6.22{\pm}0.25%$, which increased to $7.17{\pm}0.20%$ and $18.1{\pm}0.42%$ in the treatment group. Exposure to 250 and 500nmol/L TSA also caused cell morphology changes with numerous floating cells. Expression of ${\beta}$-catenin, H3K9and Bax proteins was significantly increased, expression levels of CyclinD1, HDAC1, HDAC3 were decreased. Expression of ${\beta}$-catenin at the genetic level was significantly increased, with no significant difference in HDAC1and HDAC3 genes. In the cytoplasm, expression of ${\beta}$-catenin fluorescence protein was not obvious changed and in the nucleus, small amounts of green fluorescence were observed. H3K9 fluorescence protein were increased. Expression levels of the transcription factor TCF werealso increased in HepG2 cells following induction by TSA, whikle the activity of total HDACs was decreased. Conclusions: TSA inhibits HDAC activity, promotes histone acetylation, and activates Wnt/${\beta}$-catenin signaling to inhibit proliferation of HepG2 cell, arrest cell cycling and induce apoptosis.

• 생명과학회지
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• 제30권1호
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• pp.96-105
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• 2020

서투인 억제제는 유형 III 히스톤 데아세틸라제(HDAC)인 서투인을 억제하는 화합물이며, 약제학적 및 치료학적 가치를 갖는다. 합성 서투인 억제제는 효모 S. cerevisiae 에서 세포-기반 스크린을 사용하여 발견되었고 특성화되었으며 서투인의 기능과 관련된 노화, 발암 및 당뇨병을 연구하는데 사용되었다. 의학 분야에서 합성 서투인 억제제는 보다 강력한 효능과 특이성을 얻기 위해 개발되어 왔다. 니코틴아미드 및 티오아세틸리신 함유 화합물, β-나프톨 함유화합물, 인돌 유도체. 수마린, 테노빈 및 그 유사체가 개발 되었다. 서투인 억제제는 식물 발달에 영향을 미치는 것으로 밝혀졌으며 식물의 화학적 유전학에 사용되었다. 그러나, 시르티놀-내성 돌연변이 체는 알데히드 옥시다제에 대한 몰리브돕테린 보조인자의 생합성 유전자에 돌연변이가 있었다. 일부 천연 플라보노이드, 카테킨 유도체 및 퀴르세틴 유도체는 서투인 억제제로서 작용하며 치료 목적을 위한 보다 강력한 억제제를 찾기 위해 연구 되고 있다. 이 리뷰에서, 서투인을 소개하면서 치료제에서 개발된 서투인 억제제를 소개한다. 서투인 억제제인 서티놀은 식물에서 화학적 유전학에 예기치 않게 사용되었습니다. 보다 강력하고 선택적인 서투인 억제제가 치료제에서 개발되어야 하고, 약학에서 개발된 다른 서투인 억제제는 식물에서 보다 진정한 서투인을 찾기 위해 사용되어야 한다.