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Because migration is highly time‐constrained and migration timing varies among individuals, the responses of migrants to food shortage at a refuelling site could differ between individuals that arrive early and late at the site. To test this hypothesis, we compared the stopover decision, in terms of occurrence and length of stay (LOS), of radiotagged Great Knots Calidris tenuirostris before (2012) and after (2015) a dramatic decline in food supply at a critical spring final pre‐breeding refuelling site in the northern Yellow Sea. The probability of occurrence at the refuelling site was consistent between the two years, whereas the average LOS significantly shortened in the year of food shortage in late‐arriving individuals. This suggests migration timing intensifies the influence of food shortage in late‐arriving individuals, which might be more sensitive and vulnerable to food shortage at refuelling sites compared with early‐arriving individuals.  相似文献   
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Du  Wenkai  Hu  Fengrong  Yuan  Suxia  Liu  Chun 《Molecular biology reports》2020,47(4):2487-2499
Molecular Biology Reports - Leaf color mutants are ideal materials for exploring plant photosynthesis mechanisms, chlorophyll biosynthetic pathways and chloroplast development. The yellow seedling...  相似文献   
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Maikottia属骨骼微细构造及其分类   总被引:1,自引:1,他引:0  
陈建强 《古生物学报》1997,36(4):446-452
Maikottia Laurusevich,1967属是泡沫珊瑚目中较特殊的类型,呈多角块状复体。经电镜研究表明,其骨骼微细构造以晶片型层状骨骼为主,隔壁刺由复式杆晶榍组成,层状骨骼包绕隔壁刺,在隔壁刺内包绕和联结单杆晶榍。体壁和横板均由层状骨骼组成。本属的纤状骨骼属较原始简单类型-晶粒和短轴晶柱,它组成复式杆晶榍内单杆晶榍的轴带,并呈分散状排列。根据该属为泡沫珊瑚类型隔壁及复式杆晶榍,将其归入泡  相似文献   
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p53 plays a pivotal role in controlling the differentiation of mesenchymal stem cells (MSCs) by regulating genes involved in cell cycle and early steps of differentiation process. In the context of osteogenic differentiation of MSCs and bone homeostasis, the osteoprotegerin/receptor activator of NF-κB ligand/receptor activator of NF-κB (OPG/RANKL/RANK) axis is a critical signaling pathway. The absence or loss of function of p53 has been implicated in aberrant osteogenic differentiation of MSCs that results in higher bone formation versus erosion, leading to an unbalanced bone remodeling. Here, we show by microCT that mice with p53 deletion systemically or specifically in mesenchymal cells possess significantly higher bone density than their respective littermate controls. There is a negative correlation between p53 and OPG both in vivo by analysis of serum from p53+/+, p53+/−, and p53−/− mice and in vitro by p53 knockdown and ChIP assay in MSCs. Notably, high expression of Opg or its combination with low level of p53 are prominent features in clinical cancer lesion of osteosarcoma and prostate cancer respectively, which correlate with poor survival. Intra-bone marrow injection of prostate cancer cells, together with androgen can suppress p53 expression and enhance local Opg expression, leading to an enhancement of bone density. Our results support the notion that MSCs, as osteoblast progenitor cells and one major component of bone microenvironment, represent a cellular source of OPG, whose amount is regulated by the p53 status. It also highlights a key role for the p53-OPG axis in regulating the cancer associated bone remodeling.Subject terms: Cell biology, Pathogenesis  相似文献   
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Plant intracellular immune receptors comprise a large number of multi-domain proteins resembling animal NOD-like receptors (NLRs). Plant NLRs typically recognize isolate-specific pathogen-derived effectors, encoded by avirulence (AVR) genes, and trigger defense responses often associated with localized host cell death. The barley MLA gene is polymorphic in nature and encodes NLRs of the coiled-coil (CC)-NB-LRR type that each detects a cognate isolate-specific effector of the barley powdery mildew fungus. We report the systematic analyses of MLA10 activity in disease resistance and cell death signaling in barley and Nicotiana benthamiana. MLA10 CC domain-triggered cell death is regulated by highly conserved motifs in the CC and the NB-ARC domains and by the C-terminal LRR of the receptor. Enforced MLA10 subcellular localization, by tagging with a nuclear localization sequence (NLS) or a nuclear export sequence (NES), shows that MLA10 activity in cell death signaling is suppressed in the nucleus but enhanced in the cytoplasm. By contrast, nuclear localized MLA10 is sufficient to mediate disease resistance against powdery mildew fungus. MLA10 retention in the cytoplasm was achieved through attachment of a glucocorticoid receptor hormone-binding domain (GR), by which we reinforced the role of cytoplasmic MLA10 in cell death signaling. Together with our data showing an essential and sufficient nuclear MLA10 activity in disease resistance, this suggests a bifurcation of MLA10-triggered cell death and disease resistance signaling in a compartment-dependent manner.  相似文献   
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