GAF domain is essential for nitrate-dependent AtNLP7 function
BMC Plant Biology, ISSN: 1471-2229, Vol: 22, Issue: 1, Page: 366
2022
- 6Citations
- 11Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations6
- Citation Indexes6
- Captures11
- Readers11
- 11
Article Description
Nitrate is an essential nutrient and an important signaling molecule in plants. However, the molecular mechanisms by which plants perceive nitrate deficiency signaling are still not well understood. Here we report that AtNLP7 protein transport from the nucleus to the cytoplasm in response to nitrate deficiency is dependent on the N-terminal GAF domain. With the deletion of the GAF domain, AtNLP7 always remains in the nucleus regardless of nitrate availability. AtNLP7 also shows reduced activation of nitrate-induced genes due to its impaired binding to the nitrate-responsive cis-element (NRE) as well as decreased growth like nlp7-1 mutant. In addition, AtNLP7 is unable to mediate the reduction of reactive oxygen species (ROS) accumulation upon nitrate treatment. Our investigation shows that the GAF domain of AtNLP7 plays a critical role in the sensing of nitrate deficiency signal and in the nitrate-triggered ROS signaling process.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85134637872&origin=inward; http://dx.doi.org/10.1186/s12870-022-03755-x; http://www.ncbi.nlm.nih.gov/pubmed/35871642; https://bmcplantbiol.biomedcentral.com/articles/10.1186/s12870-022-03755-x; https://dx.doi.org/10.1186/s12870-022-03755-x
Springer Science and Business Media LLC
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