Physiological and interactomic analysis reveals versatile functions of Arabidopsis 14-3-3 quadruple mutants in response to Fe deficiency

J. Gao, P.J.M. van Kleeff, K.W. Li, A.H. de Boer

Research output: Contribution to JournalArticleAcademicpeer-review

Abstract

© 2021, The Author(s).To date, few phenotypes have been described for Arabidopsis 14-3-3 mutants or the phenotypes showing the role of 14-3-3 in plant responding to abiotic stress. Although one member of the 14-3-3 protein family (14-3-3 omicron) was shown to be involved in the proper operation of Fe acquisition mechanisms at physiological and gene expression levels in Arabidopsis thaliana, it remains to be explored whether other members play a role in regulating iron acquisition. To more directly and effectively observe whether members of 14-3-3 non-epsilon group have a function in Fe-deficiency adaptation, three higher order quadruple KOs, kappa/lambda/phi/chi (klpc), kappa/lambda/upsilon/nu(klun), and upsilon/nu/phi/chi (unpc) were generated and studied for physiological analysis in this study. The analysis of iron-utilization efficiency, root phenotyping, and transcriptional level of Fe-responsive genes suggested that the mutant with kl background showed different phenotypes from Wt when plants suffered Fe starved, while these phenotypes were absent in the unpc mutant. Moreover, the absence of the four 14-3-3 isoforms in the klun mutant has a clear impact on the 14-3-3 interactome upon Fe deficiency. Dynamics of 14-3-3-client interactions analysis showed that 27 and 17 proteins differentially interacted with 14-3-3 in Wt and klun roots caused by Fe deficiency, respectively. Many of these Fe responsive proteins have a role in glycolysis, oxidative phosphorylation and TCA cycle, the FoF1-synthase and in the cysteine/methionine synthesis. A clear explanation for the observed phenotypes awaits a more detailed analysis of the functional aspects of 14-3-3 binding to the target proteins identified in this study.
Original languageEnglish
Article number15551
JournalScientific Reports
Volume11
Issue number1
DOIs
Publication statusPublished - 1 Dec 2021

Funding

We thank Ning Chen (Department of Molecular and Cellular Neurobiology, Faculty of Earth and Life Sciences, Vrije Universiteit Amsterdam) for her technical assistance with this work. The project was supported by a grant from the Netherlands Organization for Scientific Research (NWO; 817.02.006) to A.H. de Boer, and a grant from National Natural Science Foundation of China (No. 31802146) to Jing Gao.

FundersFunder number
National Natural Science Foundation of China31802146
Nederlandse Organisatie voor Wetenschappelijk Onderzoek817.02.006

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