Abstract

Seedling emergence is a pivotal step of plant survival, requiring rapid hypocotyl elongation for soil penetration 1 , 2 . This energy-demanding process necessitates active mitochondrial respiration, which inevitably induces oxidative damage 3 , 4 , 5 , 6 . Plants have therefore evolved a quality-control mechanism that selectively removes dysfunctional mitochondria through the mitophagy pathway. Here we identified SPL2, a mitochondrial E3 ligase that is essential for hypocotyl elongation and seedling emergence through degrading mitochondrial outer membrane proteins, such as TRB1 and FIS1A. Intriguingly, these proteins also interact with an endoplasmic reticulum (ER) protein, VAP27-1, forming a complex at the ER–mitochondria contact sites, which is essential for mitophagy initiation. The spl2 mutant exhibits enhanced ER–mitochondrial tethering and mitophagy activation, whereas the overexpression of SPL2 has the opposite effects. The expression of SPL2 increases after light perception, in agreement with the reduced mitophagy. Collectively, our findings reveal mechanistic insights into seedling emergence, which is coordinated through protein ubiquitination, ER–mitochondrial interaction and mitophagy.