Arabidopsis mitochondrial protein TIM50 affects hypocotyl cell elongation through intracellular ATP level

The plant hypocotyl is an excellent model for the analysis of cell elongation. We have characterized a knockout mutant of the Arabidopsis TIM50 gene that showed a reduction in the hypocotyls length of etiolated seedlings. We also found that a knockout of TIM50 caused enlargement and deformation of the mitochondrial structure and a reduction in intracellular ATP levels. TIM50 is a component of the mitochondrial TIM23 inner membrane protein complex and is involved in the import of mitochondrial proteins. The short hypocotyl phenotype was recovered by the addition of Compound C, an inhibitor of AMPK. Thus, the mitochondrial ATP level controls cell elongation in Arabidopsis hypocotyls through possible signaling via AMPK.

► The Knock out mutant of Arabidopsis Tim50 gene showed reduction in hypocotyl length.
► The mutant also showed reduction in polyploidy and Intracellular ATP levels.
► AtTim50 gene was localized in mitochondria.
► Compound C, an inhibitor of AMPK recovered the short hypocotyl phenotype.