RECG maintains plastid and mitochondrial genome stability by suppressing extensive recombination between short dispersed repeats.

Maintenance of plastid and mitochondrial genome stability is crucial for photosynthesis and respiration, respectively. Recently, we have reported that RECA1 maintains mitochondrial genome stability by suppressing gross rearrangements induced by aberrant recombination between short dispersed repeats in the moss Physcomitrella patens. In this study, we studied a newly identified P. patens homolog of bacterial RecG helicase, RECG, some of which is localized in both plastid and mitochondrial nucleoids. RECG partially complements recG deficiency in Escherichia coli cells. A knockout (KO) mutation of RECG caused characteristic phenotypes including growth delay and developmental and mitochondrial defects, which are similar to those of the RECA1 KO mutant. The RECG KO cells showed heterogeneity in these phenotypes. Analyses of RECG KO plants showed that mitochondrial genome was destabilized due to a recombination between 8-79 bp repeats and the pattern of the recombination partly differed from that observed in the RECA1 KO mutants. The mitochondrial DNA (mtDNA) instability was greater in severe phenotypic RECG KO cells than that in mild phenotypic ones. This result suggests that mitochondrial genomic instability is responsible for the defective phenotypes of RECG KO plants. Some of the induced recombination caused efficient genomic rearrangements in RECG KO mitochondria. Such loci were sometimes associated with a decrease in the levels of normal mtDNA and significant decrease in the number of transcripts derived from the loci. In addition, the RECG KO mutation caused remarkable plastid abnormalities and induced recombination between short repeats (12-63 bp) in the plastid DNA. These results suggest that RECG plays a role in the maintenance of both plastid and mitochondrial genome stability by suppressing aberrant recombination between dispersed short repeats; this role is crucial for plastid and mitochondrial functions.

The effect of 10-degree leg elevation and 30-degree head elevation on body displacement and sacral interface pressures over a 2-hour period.

OBJECTIVE: This pilot study was undertaken to determine the effects of a 10-degree leg elevation for 30-degree head-up position on body displacement and sacral interface pressure for 2 hours. DESIGN: The study used a comparative, quasi-experimental design with repeated measures. SETTINGS AND SUBJECTS: A convenience sample of 10 healthy Japanese women was used. INSTRUMENTS: Body displacement was defined as the difference over time between the top edge of the mattress and subject's acromion and was measured every 10 minutes by tape measure (in centimeters). Sacral interface pressure was measured every 10 minutes using a pneumatic pressure sensor. METHODS: The subject was placed supine on a standard hospital bed. The head of the bed was then elevated to 30 degrees according to 2 protocols: (1) supine for 10 minutes without leg elevation alternating with 10 minutes of side-lying, or (2) supine for 10 minutes with leg elevation at 10 degrees alternating with side-lying every 10 minutes. Body displacement and mean sacral interface pressures in both protocols were compared by using repeated measures analysis of variance. RESULTS: The 30-degree head-up position with 10-degree leg elevation significantly reduced the amount of body displacement at the acromion compared with no elevation of the legs. There were no significant differences in mean sacral interface pressure in either position. CONCLUSION: Leg elevation at 10 degrees in the 30-degree head-up position was effective for reducing body displacement at the acromion; it was not effective for reducing sacral interface pressures.