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Over-expression of GmHAL3 modulates salt stresses tolerance in transgenic arabidopsis
Na Guo,Ming-xia Wang,Chen-chen Xue,Dong Xue,Jin-yan Xu,Hai-tang Wang,Jun-Yi Gai,Han Xing,Jin-ming Zhao;Han Xing 한국식물학회 2016 Journal of Plant Biology Vol.59 No.5
The halotolerance protein HAL3, also known as SIS2, is a yeast protein that regulates the cell cycle and tolerance to salt stress through inhibition of the Ppz1 type 1 protein phosphatase. Although the roles of HAL3 have been demonstrated during the growth, development, and stress adaptation of Arabidopsis thaliana and Nicotiana tabacum, the function of HAL3 in other plant species, including soybean (Glycine max), has not been elucidated. In this study, GmHAL3a and GmHAL3b were isolated from Glycine max, and their roles were analyzed. GmHAL3a and GmHAL3b transcripts were detected in the roots, stems, leaves and seeds, with higher levels in the roots, and were induced by sodium chloride (NaCl), lithium chloride (LiCl), sorbitol, cold and ABA treatment. Overexpression of GmHAL3a or GmHAL3b in Arabidopsis accelerated the onset of flowering and resulted in more vigorous seed germination and increased tolerance to NaCl, LiCl, and sorbitol stress in seedlings, compared with wild type (WT) and empty vector control (VC) plants. Transgenic Arabidopsis plants accumulated proline and eliminated superoxide radical (O2 −) in response to the stress. In addition, transcription levels of the stress-related genes RD22 and P5CS1 were substantially higher in transgenic Arabidopsis than in WT and VC plants. Taken together, the data indicate that GmHAL functions as a positive regulator of the response to salt, lithium cations and sorbitol stress.
Xue-Yong Zhang,Ying-Na Jian,Hong Duo,Xiu-Ying Shen,Yi-Juan Ma,Yong Fu,Zhi-Hong Guo 대한기생충학ㆍ열대의학회 2019 The Korean Journal of Parasitology Vol.57 No.4
Coenurosis is an important zoonotic helminthic disease caused by the larval stage of the tapeworm Taenia multiceps. This parasite typically infects the brain of the intermediate hosts, including sheep, goat, cattle and even hu- mans. We report a case of T. multiceps infection in a yak confirmed by clinical symptoms, morphological characteristics, and molecular and phylogenetic analyses. The coenurus was thin-walled, whitish, and spherical in shape with a diameter of 10 cm. The parasite species was identified as T. multiceps by PCR amplification and sequencing of the 18S rRNA, cox1 and nad1 genes. Three gene sequences all showed high homology (all above 97%) with the reference sequences from different hosts. Moreover, phylogenetic reconstructions with the 3 published Taenia gene sequences confirmed that the Qinghai yak isolate was closely related to T. multiceps. Although there are advanced diagnosis and treatment meth- ods for coenurosis, early infection is difficult to diagnose. Importantly, the findings of yak infection case should not be ig- nored due to its zoonotic potential.
Li Na,Guo Xue-Yuan,Zhou Jian,Yan Xian-Liang,Yu Fang-Fang 한국조직공학과 재생의학회 2021 조직공학과 재생의학 Vol.18 No.5
BACKGROUND: We previously found that atorvastatin (ATV) enhanced mesenchymal stem cells (MSCs) migration, by a yet unknown mechanism. CXC chemokine receptor 4 (CXCR4) is critical to cell migration and regulated by microRNA-146a (miR-146a). Therefore, this study aimed to assess whether ATV ameliorates MSCs migration through miR-146a/CXCR4 signaling. METHODS: Expression of CXCR4 was evaluated by flow cytometry. Expression of miR-146a was examined by reverse transcription-quantitative polymerase chain reaction. A transwell system was used to assess the migration ability of MSCs. Recruitment of systematically delivered MSCs to the infarcted heart was evaluated in Sprague–Dawley rats with acute myocardial infarction (AMI). Mimics of miR-146a were used in vitro, and miR-146a overexpression lentivirus was used in vivo, to assess the role of miR-146a in the migration ability of MSCs. RESULTS: The results showed that ATV pretreatment in vitro upregulated CXCR4 and induced MSCs migration. In addition, flow cytometry demonstrated that miR-146a mimics suppressed CXCR4, and ATV pretreatment no longer ameliorated MSCs migration because of decreased CXCR4. In the AMI model, miR-146a-overexpressing MSCs increased infarct size and fibrosis. CONCLUSION: The miR-146a/CXCR4 signaling pathway contributes to MSCs migration and homing induced by ATV pretreatment. miR-146a may be a novel therapeutic target for stimulating MSCs migration to the ischemic tissue for improved repair.