Photosynthesis requires the incorporation of iron (Fe) into enzyme complexes. Nitric
oxide (NO) is confirmed to impact the Fe homeostasis of mesophyll cells. High expression
of the NO production elements precedes developmental senescence, and plastidial NO
production is enhanced under Fe limited conditions. Nevertheless, the role of NO induced
regulation in plastidial Fe homeostasis remained poorly known. S-nitrosoglutathione
(GSNO) is a key transmitter of NO signal that is eliminated by GSNO reductase (GSNOR).
Cryosectioned mesophyll cells of early senescent Arabidopsis thaliana line leaves
affected in GSNOR (deficient: gsnor1-3; and overexpressing: 35::FLAG::GSNOR) and in
NO biosynthesis (noa1) were analysed using particle induced X-ray emission (μPIXE),
and low energy X-ray fluorescence microscopy (LEXRF). K-means clustering of the Fe
signal distribution revealed that perturbed both GSNOR overexpression and its defect
resulted in a lowered plastidial Fe accumulation in the early senescent stage, also
confirmed by the Fe content of isolated chloroplasts and the lowered expression of
plastidial Fe acquisition elements indicating that NO signaling has a dose dependent,
Janus-faced impact on the plastidial Fe accumulation.
This work was supported by the grant K-135607 of NKFIH, Hungary. Á.S. was supported
by the János Bolyai Scholarship of the Hungarian Academy of Sciences (BO-00113-23-8).
Instrument center access was financed under ReMade@ARI PID 34653 (financed as part
of HORIZON-INFRA-2021-SERV-01, 101058414, 10039728 and 22.0018). We acknowledge Elettra-Sincrotrone,
Trieste, Italy for the beam time access (20245567).
