Specific delivery of AtBT1 to mitochondria complements the aberrant growth and sterility phenotype of homozygous Atbt1 Arabidopsis mutants.

It has been shown that homozygous AtBT1::T-DNA Arabidopsis mutants display an aberrant growth and sterility phenotype, and that AtBT1 is a carrier that is exclusively localized to the inner plastidial envelope and is required for export of newly synthesized adenylates into the cytosol. However, a recent demonstration that AtBT1 is localized to both plastids and mitochondria suggested that plastidic AtBT1 is not necessary for normal growth and fertility of Arabidopsis. To test this hypothesis, we produced and characterized homozygous AtBT1::T-DNA mutants stably expressing either dually localized AtBT1 or AtBT1 specifically localized to the mitochondrial compartment. These analyses revealed that the aberrant growth and sterility phenotype of homozygous AtBT1::T-DNA mutants was complemented when expressing both the dual-targeted AtBT1 and AtBT1 specifically delivered to mitochondria. These data confirm that (i) plastidic AtBT1 is not strictly required for normal growth and fertility of the plant, and (ii) specific delivery of AtBT1 to mitochondria is enough to complement the aberrant growth and sterility phenotype of homozygous AtBT1::T-DNA mutants. Furthermore, data presented here question the idea that the requirement for AtBT1 is due to its involvement in transport of newly synthesized adenylates from the plastid to the cytosol, and suggest that the protein may play as yet unidentified functions in plastids and mitochondria.