エジプト紅海沿岸のマングローブ林の林分構造

Established mangrove forests along the coastal area of the Arabian Peninsula and African side of the Red Sea are uniquely different from mangrove forests in other parts of the world because of their low biodiversity and harsh habitat of arid and highly saline conditions. Therefore mangrove forests in this area appear in patchy and scattered patterns at mouths of wadi or in sheltered lagoons with rare and irregular flooding. Most of them are pure forests of Avicennia marina, occasionally mixed with Rhizophora mucronata in the southern part of the Red Sea. In this study, we analyze the forest structure of A. marina and discuss the regeneration strategy and the forest dynamics of this unique mangrove species. Three experimental plots of 1000 to 2000 trees/ha were selected from north to south along the Red Sea coast. The highest tree size (6.8m) suggested severe effects of the high salinity of the Red Sea (3.2 to 4.9%) on tree growth. Dense mantle vegetation had developed at the forest edge facing the open sea to protect the forest interior against strong waves and wind. Tree growth was also prevented by severe drought on the landside edge of the forest. All the forests had a dense seedling bank throughout the forest floor, with a very high rate of turnover and regeneration, which seldom occurred in other forests

Gain-of-function mutations in RIT1 cause Noonan syndrome, a RAS/MAPK pathway syndrome

RAS GTPases mediate a wide variety of cellular functions, including cell proliferation, survival, and differentiation. Recent studies have revealed that germline mutations and mosaicism for classical RAS mutations, including those in HRAS, KRAS, and NRAS, cause a wide spectrum of genetic disorders. These include Noonan syndrome and related disorders (RAS/mitogen-activated protein kinase [RAS/MAPK] pathway syndromes, or RASopathies), nevus sebaceous, and Schimmelpenning syndrome. In the present study, we identified a total of nine missense, nonsynonymous mutations in RIT1, encoding a member of the RAS subfamily, in 17 of 180 individuals (9%) with Noonan syndrome or a related condition but with no detectable mutations in known Noonan-related genes. Clinical manifestations in the RIT1-mutation-positive individuals are consistent with those of Noonan syndrome, which is characterized by distinctive facial features, short stature, and congenital heart defects. Seventy percent of mutation-positive individuals presented with hypertrophic cardiomyopathy; this frequency is high relative to the overall 20% incidence in individuals with Noonan syndrome. Luciferase assays in NIH 3T3 cells showed that five RIT1 alterations identified in children with Noonan syndrome enhanced ELK1 transactivation. The introduction of mRNAs of mutant RIT1 into 1-cell-stage zebrafish embryos was found to result in a significant increase of embryos with craniofacial abnormalities, incomplete looping, a hypoplastic chamber in the heart, and an elongated yolk sac. These results demonstrate that gain-of-function mutations in RIT1 cause Noonan syndrome and show a similar biological effect to mutations in other RASopathy-related genes.Yoko Aok ... Christopher Barnett ... et al