NORE1/SAUL1 integrates temperature-dependent defense programs involving SGT1b and PAD4 pathways and leaf senescence in Arabidopsis.

Leaf senescence is not only primarily governed by developmental age but also influenced by various internal and external factors. Although some genes that control leaf senescence have been identified, the detailed regulatory mechanisms underlying integration of diverse senescence-associated signals into the senescence programs remain to be elucidated. To dissect the regulatory pathways involved in leaf senescence, we isolated the not oresara1-1 (nore1-1) mutant showing accelerated leaf senescence phenotypes from an EMS-mutagenized Arabidopsis thaliana population. We found that altered transcriptional programs in defense response-related processes were associated with the accelerated leaf senescence phenotypes observed in nore1-1 through microarray analysis. The nore1-1 mutation activated defense program, leading to enhanced disease resistance. Intriguingly, high ambient temperature effectively suppresses the early senescence and death phenotypes of nore1-1. The gene responsible for the phenotypes of nore1-1 contains a missense mutation in SENESCENCE-ASSOCIATED E3 UBIQUITIN LIGASE 1 (SAUL1), which was reported as a negative regulator of premature senescence in the light intensity- and PHYTOALEXIN DEFICIENT 4 (PAD4)-dependent manner. Through extensive double mutant analyses, we recently identified suppressor of the G2 Allele of SKP1b (SGT1b), one of the positive regulators for disease resistance conferred by many resistance (R) proteins, as a downstream signaling component in NORE1-mediated senescence and cell death pathways. In conclusion, NORE1/SAUL1 is a key factor integrating signals from temperature-dependent defense programs and leaf senescence in Arabidopsis. These findings provide a new insight that plants might utilize defense response program in regulating leaf senescence process, possibly through recruiting the related genes during the evolution of the leaf senescence program.

Hemodynamic effects of continuous intravenous injection and bolus plus continuous intravenous injection of oxytocin in cesarean section.

BACKGROUND: Oxytocin may cause adverse cardiovascular effects, including tachycardia and hypotension, whereas the optimal dose of oxytocin at elective cesarean section is unclear. To determine the lowest effective dose of oxytocin, we studied the hemodynamic effects of three doses during spinal anesthesia for elective single cesarean delivery. METHODS: Sixty women received oxytocin by continuous (0.5 IU/min) or bolus-continuous (2 or 5 IU prior to 0.25 IU/min continuous intravenous injection) intravenous injection after clamping of the umbilical cord. We compared changes in heart rate (HR), mean arterial pressure (MAP) and estimated blood loss (EBL). Uterine tone (UT) was assessed by palpation on a linear analog scale (LAS) at 5, 10, 15, 20 and 25 minutes after the oxytocin injection. In addition, oxytocin-related side-effects such as nausea and vomiting were recorded. RESULTS: Marked hemodynamic changes such as HR and MAP occurred in the bolus-continuous groups but not in the continuous groups. Although we were not able to observe a variation of EBL in each group, the UT significantly increased in the bolus-continuous groups when compared with that the continuous groups. In addition, the hemodynamic changes such as HR and MAP were lower in the two IU bolus-continuous group than those in the five IU group. CONCLUSIONS: Although bolus-continuous injection of oxytocin resulted in more hemodynamic changes than continuous injection, bolus-continuous injection had a greater effect on uterine contraction. Furthermore, two IU bolus-continuous injection showed lower hemodynamic changes than in the five IU bolus-continuous injection.