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

Abstract

Kirchberger et al. (2008) have shown that homozygous AtBT1::T-DNA Arabidopsis mutants display aberrant growth and sterility phenotype , and provided evidence that AtBT1 is a carrier exclusively localized to the inner plastidial envelope that is strictly required for the export of newly synthesized adenylates into the cytosol. However, the recent demonstration that AtBT1 is dually localized to plastids and mitochondria (Bahaji et al., 2011) has prompted the hypothesis that plastidic AtBT1 would not be essential for normal growth and fertility of Arabidopsis. To test this hypothesis we produced and characterized homozygous AtBT1::T-DNA mutants stably expressing either the dually localized AtBT1, or AtBT1 specifically localized in 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 the AtBT1 specifically delivered to mitochondria. The overall data thus show that (a) AtBT1 is an essential gene, (b) plastidic AtBT1 is not strictly required for normal growth and fertility of the plant, and (c) 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 in this work question the idea that AtBT1 essentiality is due to its involvement in the transport of newly synthesized adenylates from the plastid to the cytosol, and suggest that the protein plays yet to be identified overlapping function s in plastids and mitochondria.