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- Büntgen, Ulf, et al.
(author)
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Global tree-ring response and inferred climate variation following the mid-thirteenth century Samalas eruption
- 2022
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In: Climate Dynamics. - : Springer Science and Business Media LLC. - 0930-7575 .- 1432-0894. ; 59:1-2, s. 531-546
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Journal article (peer-reviewed)abstract
- The largest explosive volcanic eruption of the Common Era in terms of estimated sulphur yield to the stratosphere was identified in glaciochemical records 40 years ago, and dates to the mid-thirteenth century. Despite eventual attribution to the Samalas (Rinjani) volcano in Indonesia, the eruption date remains uncertain, and the climate response only partially understood. Seeking a more global perspective on summer surface temperature and hydroclimate change following the eruption, we present an analysis of 249 tree-ring chronologies spanning the thirteenth century and representing all continents except Antarctica. Of the 170 predominantly temperature sensitive high-frequency chronologies, the earliest hints of boreal summer cooling are the growth depressions found at sites in the western US and Canada in 1257 CE. If this response is a result of Samalas, it would be consistent with an eruption window of circa May-July 1257 CE. More widespread summer cooling across the mid-latitudes of North America and Eurasia is pronounced in 1258, while records from Scandinavia and Siberia reveal peak cooling in 1259. In contrast to the marked post-Samalas temperature response at high-elevation sites in the Northern Hemisphere, no strong hydroclimatic anomalies emerge from the 79 precipitation-sensitive chronologies. Although our findings remain spatially biased towards the western US and central Europe, and growth-climate response patterns are not always dominated by a single meteorological factor, this study offers a global proxy framework for the evaluation of paleoclimate model simulations.
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| 2. |
- Martrat, Griselda, et al.
(author)
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Exploring the link between MORF4L1 and risk of breast cancer
- 2011
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In: Breast Cancer Research. - : Springer Science and Business Media LLC. - 1465-5411 .- 1465-542X. ; 13:2
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Journal article (peer-reviewed)abstract
- Introduction: Proteins encoded by Fanconi anemia (FA) and/or breast cancer (BrCa) susceptibility genes cooperate in a common DNA damage repair signaling pathway. To gain deeper insight into this pathway and its influence on cancer risk, we searched for novel components through protein physical interaction screens. Methods: Protein physical interactions were screened using the yeast two-hybrid system. Co-affinity purifications and endogenous co-immunoprecipitation assays were performed to corroborate interactions. Biochemical and functional assays in human, mouse and Caenorhabditis elegans models were carried out to characterize pathway components. Thirteen FANCD2-monoubiquitinylation-positive FA cell lines excluded for genetic defects in the downstream pathway components and 300 familial BrCa patients negative for BRCA1/2 mutations were analyzed for genetic mutations. Common genetic variants were genotyped in 9,573 BRCA1/2 mutation carriers for associations with BrCa risk. Results: A previously identified co-purifying protein with PALB2 was identified, MRG15 (MORF4L1 gene). Results in human, mouse and C. elegans models delineate molecular and functional relationships with BRCA2, PALB2, RAD51 and RPA1 that suggest a role for MRG15 in the repair of DNA double-strand breaks. Mrg15-deficient murine embryonic fibroblasts showed moderate sensitivity to g-irradiation relative to controls and reduced formation of Rad51 nuclear foci. Examination of mutants of MRG15 and BRCA2 C. elegans orthologs revealed phenocopy by accumulation of RPA-1 (human RPA1) nuclear foci and aberrant chromosomal compactions in meiotic cells. However, no alterations or mutations were identified for MRG15/MORF4L1 in unclassified FA patients and BrCa familial cases. Finally, no significant associations between common MORF4L1 variants and BrCa risk for BRCA1 or BRCA2 mutation carriers were identified: rs7164529, P-trend = 0.45 and 0.05, P-2df = 0.51 and 0.14, respectively; and rs10519219, P-trend = 0.92 and 0.72, P-2df = 0.76 and 0.07, respectively. Conclusions: While the present study expands on the role of MRG15 in the control of genomic stability, weak associations cannot be ruled out for potential low-penetrance variants at MORF4L1 and BrCa risk among BRCA2 mutation carriers.
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