Two Nucleoporin98 homologous genes jointly participate in the regulation of starch degradation to repress senescence in Arabidopsis

Background Starch is synthesized during daylight for temporary storage in leaves and then degraded during the subsequent night to support plant growth and development. Impairment of starch degradation leads to stunted growth, even senescence and death. The nuclear pore complex is involved in many cellular processes, but its relationship with starch degradation has been unclear until now. We previously identified that twoNucleoporin98genes (Nup98aandNup98b) redundantly regulate flowering via theCONSTANS(CO)-independent pathway inArabidopsis thaliana. The double mutant also shows severe senescence phenotypes. Results We find thatNucleoporin 98participates in the regulation of sugar metabolism in leaves and is also involved in senescence regulation inArabidopsis. We show thatNup98aandNup98bfunction redundantly at different stages of starch degradation. Thenup98a-1 nup98b-1double mutant accumulates more starch, showing a severe early senescence phenotype compared to wild type plants. The expression of marker genes related to starch degradation is impaired in thenup98a-1 nup98b-1double mutant, and marker genes of carbon starvation and senescence express their products earlier and in higher abundance than in wild type plants, suggesting that abnormalities in energy metabolism are the main cause of senescence in the double mutant. Addition of sucrose to the growth medium rescues early senescence phenotypes of thenup98a-1 nup98b-1mutant. Conclusions Our results provide evidence for a novel role of the nuclear pore complex in energy metabolism related to growth and development, in whichNup98functions in starch degradation to control growth regulation inArabidopsis.