久发体育(2026已更新)新人权益

Recently, Professor Sun Jiaqi’s team from the School of Life Sciences at Shandong University published a research article entitled “ER-mitochondria tether ML1 coordinates peripheral fission and wholesale mitophagy for plant adaptation to carbon starvation” in Science Advances. This study reveals that the carbon starvation-induced ER–mitochondria tethering protein ML1 (mitochondria–ER linker 1) coordinates mitochondrial fission mode switching and wholesale mitophagy at organelle contact sites, enabling rapid mitochondrial population remodeling and resource recycling for plant adaptation to carbon starvation.

As sessile organisms, plants often experience carbon limitation caused by darkness, shading, or growth in non-photosynthetic tissues. Although mitochondria generate ATP under carbon-rich conditions, their maintenance becomes energetically costly during carbon starvation, creating a metabolic paradox. Using live-cell imaging, the researchers identified two mitochondrial fission modes: central symmetric fission, which produces similarly sized daughter mitochondria, and peripheral asymmetric fission, which generates small fragments with reduced membrane potential. Under normal conditions, symmetric fission dominates (~75% of events), whereas carbon starvation triggers a rapid increase in peripheral fission from less than 10% to approximately 90% within 24 hours, revealing an active mitochondrial remodeling strategy to reduce cellular metabolic burden.

Figure 1. Live-cell imaging of Mito-GFP-labeled mitochondria undergoing central symmetric fission (A) and peripheral asymmetric fission (B) in Arabidopsis root cells under normal growth conditions.

Contrary to the conventional view, carbon starvation-induced autophagy does not selectively target damaged, small mitochondrial fragments. Instead, it preferentially removes medium-sized mitochondria with intact membrane potential, while small fragments and excessively elongated mitochondria are largely spared. This damage-independent “wholesale” mitochondrial clearance is severely impaired in autophagy-deficient mutants. Rather than serving primarily as a mitochondrial quality-control mechanism, this process functions to rapidly reduce the overall mitochondrial burden and recycle cellular resources, thereby achieving a strategy of “resource conservation and recovery.” A portion of the small mitochondrial fragments with reduced membrane potential is eliminated through autophagy and can be replenished after carbon availability is restored.

Figure 2. Real-time imaging of wholesale mitophagy in Mito-GFP/mCherry-ATG8e co-expressing Arabidopsis root cells after 12 h of carbon starvation. A medium-sized mitochondrion is progressively engulfed by an ATG8e-positive autophagic structure.

During carbon starvation, ML1 accumulates at ER–mitochondria contact sites and coordinates two simultaneous processes: promoting peripheral fission to isolate damaged regions and recruiting the autophagy-related protein ATG18a to initiate mitophagy, thereby achieving an efficient “cut-and-clear” mitochondrial recycling process. Mutants lacking ML1 or key autophagy genes exhibit enhanced chlorosis and severe growth inhibition under carbon starvation. This pathway is insensitive to nitrogen starvation, highlighting its specific role in carbon starvation adaptation. This study challenges the traditional view of mitophagy as primarily a damage-removal mechanism and introduces the concept of “metabolic adaptive mitophagy.” It integrates mitochondrial fission mode switching, organelle contact sites, and selective autophagy into a unified regulatory network, providing new insights into how plants remodel organelle homeostasis to adapt to metabolic stress.

Figure 3. Working model illustrating ML1-mediated coordinated mitochondrial remodeling during carbon starvation.

This work was supported by funding from the National Natural Science Foundation of China, the Shandong Provincial Natural Science Foundation for Young Scholars, the Guangdong Basic and Applied Basic Research Foundation, and the Qingdao Postdoctoral Research Program.