Climate change-induced greening on the Tibetan Plateau modulated by mountainous characteristics

International audienceGlobal terrestrial vegetation is greening, particularly in mountain areas, providing strong feedbacks to a series of ecosystem processes. This greening has been primarily attributed to climate change. However, the spatial variability and magnitude of such greening do not synchronize with those of climate change in mountain areas. By integrating two data sets of satellite-derived normalized difference vegetation index (NDVI) values, which are indicators of vegetation greenness, in the period 1982-2015 across the Tibetan Plateau (TP), we test the hypothesis that climate-changeinduced greening is regulated by terrain, baseline climate and soil properties. We find a widespread greening trend over 91% of the TP vegetated areas, with an average greening rate (i.e. increase in NDVI) of 0.011 per decade. The linear mixed-effects model suggests that climate change alone can explain only 26% of the variation in the observed greening. Additionally, 58% of the variability can be explained by the combination of the mountainous characteristics of terrain, baseline climate and soil properties, and 32% of this variability was explained by terrain. Path analysis identified the interconnections of climate change, terrain, baseline climate and soil in determining greening. Our results demonstrate the important role of mountainous effects in greening in response to climate change

Noncanonical and canonical splice sites: a novel mutation at the rare noncanonical splice-donor cut site (IVS4+1A>G) of SEDL causes variable splicing isoforms in X-linked spondyloepiphyseal dysplasia tarda

X-linked spondyloepiphyseal dysplasia tarda can be caused by mutations in the SEDL gene. This study describes an interesting novel mutation (IVS4+1A>G) located exactly at the rare noncanonical AT–AC consensus splicing donor point of SEDL, which regained the canonical GT–AG consensus splicing junction in addition to several other rarer noncanonical splice patterns. The mutation activated several cryptic splice sites and generated the production of seven erroneous splicing isoforms, which we confirmed by sequencing of RT-PCR products and resequencing of cDNA clones. All the practical splice donors/acceptors were further assessed using FSPLICE 1.0 and SPL(M) Platforms to predict potential splice sites in genomic DNA. Subsequently, the expression levels of SEDL among the affected patients, carriers and controls were estimated using real-time quantitative PCR. Expression analyses showed that the expression levels of SEDL in both patients and carriers were decreased. Taken together, these results illustrated how disruption of the AT donor site in a rare AT–AC intron, leading to a canonical GT donor site, resulted in a multitude of aberrant transcripts, thus impairing exon definition. The unexpected splicing patterns resulting from the special mutation provide additional challenges and opportunities for understanding splicing mechanisms and specificity