| 1. |
- Ailizati, Aili, et al.
(författare)
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An Arabidopsis NAC domain transcriptional activator VND7 negatively regulates VNI2 expression
- 2021
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Ingår i: Plant Biotechnology. - : Japanese Society for Plant Cell and Molecular Biology. - 1342-4580 .- 1347-6114. ; 38:4, s. 415-420
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Tidskriftsartikel (refereegranskat)abstract
- A NAC domain transcription factor, VND-INTERACTING2 (VNI2) is originally isolated as an interacting protein with another NAC domain transcription factor, VASCULAR-RELATED NAC-DOMAIN7 (VND7), a master regulator of xylem vessel element differentiation. VND7 directly or indirectly induces expression of a number of genes associated with xylem vessel element differentiation, while VNI2 inhibits the transcriptional activation activities of VND7 by forming a protein complex. VNI2 is expressed at an earlier stage of xylem vessel element differentiation than VND7. Here, to investigate whether VND7 also affects VNI2, a transient expression assay was performed. We demonstrated that VND7 downregulated VNI2 expression. Other transcription factors involved in xylem vessel formation did not show the negative regulation of VNI2 expression. Rather, MYB83, a downstream target of VND7, upregulated VNI2 expression. By using the deletion series of the VNI2 promoter, a 400 bp region was identified as being responsible for downregulation by VND7. These data suggested that VND7 and VNI2 mutually regulate each other, and VNI2 expression is both positively and negatively regulated in the transcriptional cascade.
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| 2. |
- Ailizati, Aili, et al.
(författare)
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VND-INTERACTING2 effectively inhibits transcriptional activities of VASCULAR-RELATED NAC-DOMAIN7 through a conserved sequence
- 2022
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Ingår i: Plant Biotechnology. - : Japanese Society for Plant Cell and Molecular Biology. - 1342-4580 .- 1347-6114. ; 39:2, s. 147-153
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Tidskriftsartikel (refereegranskat)abstract
- An Arabidopsis NAC domain transcription factor VND-INTERACTING2 (VNI2) was originally isolated as an interacting protein with another NAC domain transcription factor, VASCULAR-RELATED NAC-DOMAIN7 (VND7), a master regulator of xylem vessel element differentiation. VNI2 inhibits transcriptional activation activity of VND7 by forming a protein complex. Here, to obtain insights into how VNI2 regulates VND7, we tried to identify the amino acid region of VNI2 required for inhibition of VND7. VNI2 has an amino acid sequence similar to the ETHYLENE-RESPONSIVE ELEMENT BINDING FACTOR (ERF)-associated amphiphilic repression (EAR) motif, conserved in transcriptional repressors, at the C-terminus. A transient expression assay showed that the EAR-like motif of VNI2 was not required for inhibition of VND7. The C-terminal deletion series of VNI2 revealed that 10 amino acid residues, highly conserved in the VNI2 orthologs contributed to effective repression of the transcriptional activation activity of VND7. Observation of transgenic plants ectopically expressing VNI2 showed that the identified 10 amino acid sequence strongly affected xylem vessel formation and plant growth. These data indicated that the 10 amino acid sequence of VNI2 has an important role in its transcriptional repression activity and negative regulation of xylem vessel formation.
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| 3. |
- Nagahage, Isura Sumeda Priyadarshana, et al.
(författare)
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An Arabidopsis NAC domain transcription factor, ATAF2, promotes age-dependent and dark-induced leaf senescence
- 2020
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Ingår i: Physiologia Plantarum. - : Blackwell Publishing. - 0031-9317 .- 1399-3054. ; 170:2, s. 299-308
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Tidskriftsartikel (refereegranskat)abstract
- Leaf senescence is controlled developmentally and environmentally and is affected by numerous genes, including transcription factors. An Arabidopsis NAC domain transcription factor, ATAF2, is known to regulate biotic stress responses. Recently, we have demonstrated that ATAF2 upregulates ORE1, a key regulator of leaf senescence. Here, to investigate the function of ATAF2 in leaf senescence further, we generated and analyzed overexpressing transgenic and T-DNA inserted mutant lines. Transient expression analysis indicated that ATAF2 upregulates several NAC domain transcription factors that regulate senescence. Indeed, ATAF2 overexpression induced the expression of senescence-related genes, thereby accelerating leaf senescence, whereas the expression of such genes in ataf2 mutants was lower than that of wild-type plants. Furthermore, the ataf2 mutants exhibited significant delays in dark-induced leaf senescence. It was also found that ATAF2 induces the expression of transcription factors, which both promotes and represses leaf senescence. The present study demonstrates that ATAF2 promotes leaf senescence in response to developmental and environmental signals.
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| 4. |
- Nagahage, Isura Sumeda Priyadarshana, et al.
(författare)
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NAC domain transcription factors VNI2 and ATAF2 form protein complexes and regulate leaf senescence
- 2023
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Ingår i: Plant Direct. - : John Wiley & Sons. - 2475-4455. ; 7:9
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Tidskriftsartikel (refereegranskat)abstract
- The NAM, ATAF1/2, and CUC2 (NAC) domain transcription factor VND-INTERACTING2 (VNI2) negatively regulates xylem vessel formation by interacting with another NAC domain transcription factor, VASCULAR-RELATED NAC-DOMAIN7 (VND7), a master regulator of xylem vessel formation. Here, we screened interacting proteins with VNI2 using yeast two-hybrid assay and isolated two NAC domain transcription factors, Arabidopsis thaliana ACTIVATION FACTOR 2 (ATAF2) and NAC DOMAIN CONTAINING PROTEIN 102 (ANAC102). A transient gene expression assay showed that ATAF2 upregulates the expression of genes involved in leaf senescence, and VNI2 effectively inhibits the transcriptional activation activity of ATAF2. vni2 mutants accelerate leaf senescence, whereas ataf2 mutants delay leaf senescence. In addition, the accelerated leaf senescence phenotype of the vni2 mutant is recovered by simultaneous mutation of ATAF2. Our findings strongly suggest that VNI2 interacts with and inhibits ATAF2, resulting in negatively regulating leaf senescence.
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| 5. |
- Yoshitake, Shimako, et al.
(författare)
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Correlation between the effects of local and intracerebroventricular infusions of galanin on 5-HT release studied by microdialysis, and distribution of galanin and galanin receptors in prefrontal cortex, ventral hippocampus, amygdala, hypothalamus, and striatum of awake rats
- 2014
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Ingår i: Synapse. - : John Wiley & Sons. - 0887-4476 .- 1098-2396. ; 68:5, s. 179-193
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Tidskriftsartikel (refereegranskat)abstract
- The neuropeptide galanin is implicated in regulation of affective behavior, including modulation of 5-HT signaling. Here, we investigated, by use of microdialysis in freely moving rats, the effects of intracerebral (i.c.) and intracerebroventricular (i.c.v.) infusions of galanin on basal extracellular 5-HT levels in medial prefrontal cortex (mPFC), CA1 area of ventral hippocampus (vHPC), central amygdaloid nucleus (CeA), ventromedial hypothalamic nucleus ventrolateral part (VMHvl), and ventromedial caudate putamen (CPu). These results were compared with a parallel immunohistochemical analysis of the distribution of galanin, 5-HT, and noradrenaline (NA) nerve terminals, and with data on galanin receptors. Galanin i.c.v. significantly decreased the 5-HT levels in mPFC to 79% and in vHPC to 72%. Local infusions of galanin caused a long-lasting decrease in 5-HT levels in vHPC to 88%, and a moderate decrease in CeA, whereas the 5-HT levels in mPFC significantly increased to 121%. These effects of i.c. galanin correlated well with the density of 5-HT and galanin nerve terminals and galanin receptors autoradiography in mPFC, vHPC, and CeA. No effects of i.c. or i.c.v. galanin on 5-HT levels were observed in CPu or VMHvl, in agreement with the low numbers of galanin-positive terminals and low/moderate galanin receptor density. Galanin was often found to coexist in NA, but could never be detected in 5-HT terminals. Together the results show a neuroanatomical correlation between the effects of galanin infusions on 5-HT release and distribution of galanin and its receptors, and that i.c.v. and i.c. administration can give opposite effects on 5-HT release.
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