Disruption of Nap14, a plastid-localized non-intrinsic ABC protein in Arabidopsis thaliana results in the over-accumulation of transition metals and in aberrant chloroplast structures.

Chloroplasts are the major sink for Fe in shoot tissues because of the requirements of the photosynthetic process and to storage in ferritins. Such requirements are common both to plastids and to their evolutionary progenitors, the cyanobacteria. Here, we examined whether iron transport mechanisms were conserved throughout the evolution of photosynthetic organisms. Comparison of the sequences of putative plastid transporters from Arabidopsis thaliana with those involved in cyanobacterial Fe transport identified two orthologs of the FutC protein, AtNAP11 and AtNAP14. To study their function, we analysed insertional mutants in the genes coding for these proteins. Both nap11/nap11 and nap14/nap14 plants exhibited severe growth defects. Significant changes in transition metal homeostasis were detected only in nap14/nap14. This mutant was found to contain approximately 18 times more Fe in the shoot tissue than in wild-type plants. The increased shoot transition metal content was accompanied by a specific loss of chloroplast structures and by a reduction in transcript levels of Fe homeostasis-related genes. Based on these results, we propose that AtNAP14 plays an important role in plastid transition metal homeostasis. One possibility is that AtNAP14 is part of a chloroplast transporter complex. Alternatively, AtNAP14 function may be in regulating transition metal homeostasis.

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