scholarly journals Heterologous Expression of a Glycine soja C2H2 Zinc Finger Gene Improves Aluminum Tolerance in Arabidopsis

2020 ◽  
Vol 21 (8) ◽  
pp. 2754
Author(s):  
Yuan-Tai Liu ◽  
Qi-Han Shi ◽  
He-Jie Cao ◽  
Qi-Bin Ma ◽  
Hai Nian ◽  
...  

Aluminum (Al) toxicity limits plant growth and has a major impact on the agricultural productivity in acidic soils. The zinc-finger protein (ZFP) family plays multiple roles in plant development and abiotic stresses. Although previous reports have confirmed the function of these genes, their transcriptional mechanisms in wild soybean (Glycine soja) are unclear. In this study, GsGIS3 was isolated from Al-tolerant wild soybean gene expression profiles to be functionally characterized in Arabidopsis. Laser confocal microscopic observations demonstrated that GsGIS3 is a nuclear protein, containing one C2H2 zinc-finger structure. Our results show that the expression of GsGIS3 was of a much higher level in the stem than in the leaf and root and was upregulated under AlCl3, NaCl or GA3 treatment. Compared to the control, overexpression of GsGIS3 in Arabidopsis improved Al tolerance in transgenic lines with more root growth, higher proline and lower Malondialdehyde (MDA) accumulation under concentrations of AlCl3. Analysis of hematoxylin staining indicated that GsGIS3 enhanced the resistance of transgenic plants to Al toxicity by reducing Al accumulation in Arabidopsis roots. Moreover, GsGIS3 expression in Arabidopsis enhanced the expression of Al-tolerance-related genes. Taken together, our findings indicate that GsGIS3, as a C2H2 ZFP, may enhance tolerance to Al toxicity through positive regulation of Al-tolerance-related genes.

2008 ◽  
Vol 28 (7) ◽  
pp. 2358-2367 ◽  
Author(s):  
Yong-Sik Kim ◽  
Hong Soon Kang ◽  
Ronald Herbert ◽  
Ju Youn Beak ◽  
Jennifer B. Collins ◽  
...  

ABSTRACT To obtain insight into the physiological functions of the Krüppel-like zinc finger protein Gli-similar 2 (Glis2), mice deficient in Glis2 expression were generated. Glis2 mutant (Glis2mut) mice exhibit significantly shorter life spans than do littermate wild-type (WT) mice due to the development of progressive chronic kidney disease with features resembling nephronophthisis. Glis2mut mice develop severe renal atrophy involving increased cell death and basement membrane thickening in the proximal convoluted tubules. This development is accompanied by infiltration of lymphocytic inflammatory cells and interstitial/glomerular fibrosis. The severity of the fibrosis, inflammatory infiltrates, and glomerular and tubular changes progresses with age. Blood urea nitrogen and creatinine increase, and Glis2mut mice develop proteinuria and ultimately die prematurely of renal failure. A comparison of the gene expression profiles of kidneys from 25-day-old/60-day-old WT and Glis2mut mice by microarray analysis showed increased expressions of many genes involved in immune responses/inflammation and fibrosis/tissue remodeling in kidneys of Glis2mut mice, including several cytokines and adhesion and extracellular matrix proteins. Our data demonstrate that a deficiency in Glis2 expression leads to tubular atrophy and progressive fibrosis, similar to nephronophthisis, that ultimately results in renal failure. Our study indicates that Glis2 plays a critical role in the maintenance of normal kidney architecture and functions.


2020 ◽  
Vol 21 (5) ◽  
pp. 1879 ◽  
Author(s):  
Shanshan He ◽  
Gaopeng Yuan ◽  
Shuxun Bian ◽  
Xiaolei Han ◽  
Kai Liu ◽  
...  

Major latex proteins (MLPs) play critical roles in plants defense and stress responses. However, the roles of MLPs from apple (Malus × domestica) have not been clearly identified. In this study, we focused on the biological role of MdMLP423, which had been previously characterized as a potential pathogenesis-related gene. Phylogenetic analysis and conserved domain analysis indicated that MdMLP423 is a protein with a ‘Gly-rich loop’ (GXGGXG) domain belonging to the Bet v_1 subfamily. Gene expression profiles showed that MdMLP423 is mainly expressed in flowers. In addition, the expression of MdMLP423 was significantly inhibited by Botryosphaeria berengeriana f. sp. piricola (BB) and Alternaria alternata apple pathotype (AAAP) infections. Apple calli overexpressing MdMLP423 had lower expression of resistance-related genes, and were more sensitive to infection with BB and AAAP compared with non-transgenic calli. RNA-seq analysis of MdMLP423-overexpressing calli and non-transgenic calli indicated that MdMLP423 regulated the expression of a number of differentially expressed genes (DEGs) and transcription factors, including genes involved in phytohormone signaling pathways, cell wall reinforcement, and genes encoding the defense-related proteins, AP2-EREBP, WRKY, MYB, NAC, Zinc finger protein, and ABI3. Taken together, our results demonstrate that MdMLP423 negatively regulates apple resistance to BB and AAAP infections by inhibiting the expression of defense- and stress-related genes and transcription factors.


Genomics ◽  
1995 ◽  
Vol 25 (1) ◽  
pp. 322-323 ◽  
Author(s):  
Stephanie Halford ◽  
Marie-Genevieve Mattei ◽  
Sara Daw ◽  
Peter J. Scambler

Author(s):  
Lu Xue ◽  
Hongling Qiu ◽  
Jian Ma ◽  
Mingxiong Guo ◽  
Wenxin Li

AbstractZNF300 was recently identified as a member of the human KRAB/C2H2 zinc finger protein family. Little is known about the role of ZNF300 in human gene regulation networks. In this study, the DNA-binding property of ZNF300 was further analyzed. We found that the recombinant ZNF300 could bind to the binding site 5′-GCGGGGGCG-3′ of Egr1, another member of the KRAB/C2H2 zinc finger protein family. Similarly, recombinant Egr1 also showed a similar binding affinity to the ZNF300 binding site 5′-CTGGGGGCG-3′. Bioinformatics analysis revealed that there is an overlapping ZNF300/Egr1 binding site in the human IL-2Rβ promoter region, which was previously known to be recognized by endogenous Egr1. Electrophoretic mobility shift assays showed that endogenous ZNF300 could also bind to this site. A transient transfection assay revealed that both ZNF300 and Egr1 could transactivate the IL-2Rβ promoter, and that the activation was abrogated by a mutation of residues in the overlapping ZNF300/Egr1 binding site. Co-expression of ZNF300 and Egr1 led to enhanced IL-2Rβ promoter activity. Thus, ZNF300 is likely to be another regulator of the human IL-2Rβ promoter.


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