A mutation in Arabidopsis SAL1 alters its in vitro activity against IP 3 and delays developmental leaf senescence in association with lower ROS levels

Key message Our manuscript is the first to find a link between activity of SAL1/OLD101 against IP 3 and plant leaf senescence regulation and ROS levels assigning a potential biological role for IP 3 . Abstract Leaf senescence is a genetically programmed process that limits the longevity of a leaf. We identified and analyzed the recessive Arabidopsis stay-green mutation onset of leaf death 101 ( old101 ). Developmental leaf longevity is extended in old101 plants, which coincided with higher peroxidase activity and decreased H 2 O 2 levels in young 10-day-old, but not 25-day-old plants. The old101 phenotype is caused by a point mutation in SAL1 , which encodes a bifunctional enzyme with inositol polyphosphate-1-phosphatase and 3′ (2′), 5′-bisphosphate nucleotidase activity. SAL1 activity is highly specific for its substrates 3-polyadenosine 5-phosphate (PAP) and inositol 1, 4, 5-trisphosphate (IP 3 ), where it removes the 1-phosphate group from the IP 3 second messenger. The in vitro activity of recombinant old101 protein against its substrate IP 3 was 2.5-fold lower than that of wild type SAL1 protein. However, the in vitro activity of recombinant old101 mutant protein against PAP remained the same as that of the wild type SAL1 protein. The results open the possibility that the activity of SAL1 against IP 3 may affect the redox balance of young seedlings and that this delays the onset of leaf senescence.