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991.
992.
Shirley Ang Jana Kogulanathan Gordon A. Morris M. Samil Kök Peter R. Shewry Arthur S. Tatham Gary G. Adams Arthur J. Rowe Stephen E. Harding 《European biophysics journal : EBJ》2010,39(2):255-261
A study of the heterogeneity and conformation in solution [in 70% (v/v) aq. ethanol] of gliadin proteins from wheat was undertaken
based upon sedimentation velocity in the analytical ultracentrifuge, analysis of the distribution coefficients and ellipsoidal
axial ratios assuming quasi-rigid particles, allowing for a range of plausible time-averaged hydration values. All classical
fractions (α, γ, ωslow, ωfast) show three clearly resolved components. Based on the weight-average sedimentation coefficient for each fraction and a weight-average
molecular weight from sedimentation equilibrium and/or cDNA sequence analysis, all the proteins are extended molecules with
axial ratios ranging from ~10 to 30 with α appearing the most extended and γ the least. 相似文献
993.
Catherine Coutand Malia Chevolot Andr�� Lacointe Nick Rowe Ivan Scotti 《Annals of botany》2010,105(2):341-347
Background and Aims
In rain forests, sapling survival is highly dependent on the regulation of trunk slenderness (height/diameter ratio): shade-intolerant species have to grow in height as fast as possible to reach the canopy but also have to withstand mechanical loadings (wind and their own weight) to avoid buckling. Recent studies suggest that mechanosensing is essential to control tree dimensions and stability-related morphogenesis. Differences in species slenderness have been observed among rainforest trees; the present study thus investigates whether species with different slenderness and growth habits exhibit differences in mechanosensitivity.Methods
Recent studies have led to a model of mechanosensing (sum-of-strains model) that predicts a quantitative relationship between the applied sum of longitudinal strains and the plant''s responses in the case of a single bending. Saplings of five different neotropical species (Eperua falcata, E. grandiflora, Tachigali melinonii, Symphonia globulifera and Bauhinia guianensis) were subjected to a regimen of controlled mechanical loading phases (bending) alternating with still phases over a period of 2 months. Mechanical loading was controlled in terms of strains and the five species were subjected to the same range of sum of strains. The application of the sum-of-strain model led to a dose–response curve for each species. Dose–response curves were then compared between tested species.Key Results
The model of mechanosensing (sum-of-strain model) applied in the case of multiple bending as long as the bending frequency was low. A comparison of dose–response curves for each species demonstrated differences in the stimulus threshold, suggesting two groups of responses among the species. Interestingly, the liana species B. guianensis exhibited a higher threshold than other Leguminosae species tested.Conclusions
This study provides a conceptual framework to study variability in plant mechanosensing and demonstrated interspecific variability in mechanosensing.Key words: Mechanosensing, interspecific variability, trees, lianas, rain forest, neotropical species, bending, biomechanics, Bauhinia, Eperua, Symphonia, Tachigali 相似文献994.
Sophie Lèbre Jennifer Becq Frédéric Devaux Michael PH Stumpf Gaëlle Lelandais 《BMC systems biology》2010,4(1):130
Background
Biological networks are highly dynamic in response to environmental and physiological cues. This variability is in contrast to conventional analyses of biological networks, which have overwhelmingly employed static graph models which stay constant over time to describe biological systems and their underlying molecular interactions. 相似文献995.
996.
Huntington's disease (HD) is one of several neurodegenerative disorders caused by expansion of CAG repeats in a coding gene. Somatic CAG expansion rates in HD vary between organs, and the greatest instability is observed in the brain, correlating with neuropathology. The fundamental mechanisms of somatic CAG repeat instability are poorly understood, but locally formed secondary DNA structures generated during replication and/or repair are believed to underlie triplet repeat expansion. Recent studies in HD mice have demonstrated that mismatch repair (MMR) and base excision repair (BER) proteins are expansion inducing components in brain tissues. This study was designed to simultaneously investigate the rates and modes of expansion in different tissues of HD R6/1 mice in order to further understand the expansion mechanisms in vivo. We demonstrate continuous small expansions in most somatic tissues (exemplified by tail), which bear the signature of many short, probably single-repeat expansions and contractions occurring over time. In contrast, striatum and cortex display a dramatic--and apparently irreversible--periodic expansion. Expansion profiles displaying this kind of periodicity in the expansion process have not previously been reported. These in vivo findings imply that mechanistically distinct expansion processes occur in different tissues. 相似文献
997.
Claas Wodarczyk Gianfranco Distefano Isaline Rowe Massimiliano Gaetani Barbara Bricoli Mordi Muorah Andrea Spitaleri Valeria Mannella Piero Ricchiuto Monika Pema Maddalena Castelli Ariel E. Casanova Luca Mollica Manuela Banzi Manila Boca Corinne Antignac Sophie Saunier Giovanna Musco Alessandra Boletta 《PloS one》2010,5(9)
Mutations in PKD1, the gene encoding for the receptor Polycystin-1 (PC-1), cause autosomal dominant polycystic kidney disease (ADPKD). The cytoplasmic C-terminus of PC-1 contains a coiled-coil domain that mediates an interaction with the PKD2 gene product, Polycystin-2 (PC-2). Here we identify a novel domain in the PC-1 C-terminal tail, a polyproline motif mediating an interaction with Src homology domain 3 (SH3). A screen for interactions using the PC-1 C-terminal tail identified the SH3 domain of nephrocystin-1 (NPHP1) as a potential binding partner of PC-1. NPHP1 is the product of a gene that is mutated in a different form of renal cystic disease, nephronophthisis (NPHP). We show that in vitro pull-down assays and NMR structural studies confirmed the interaction between the PC-1 polyproline motif and the NPHP1 SH3 domain. Furthermore, the two full-length proteins interact through these domains; using a recently generated model system allowing us to track endogenous PC-1, we confirm the interaction between the endogenous proteins. Finally, we show that NPHP1 trafficking to cilia does not require PC-1 and that PC-1 may require NPHP1 to regulate resistance to apoptosis, but not to regulate cell cycle progression. In line with this, we find high levels of apoptosis in renal specimens of NPHP patients. Our data uncover a link between two different ciliopathies, ADPKD and NPHP, supporting the notion that common pathogenetic defects, possibly involving de-regulated apoptosis, underlie renal cyst formation. 相似文献
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999.
1000.
David H Shu Thomas PP Ransom Colleen M O'Connell Jafna L Cox Stephanie M Kaiser Shirl A Gee Richard C Rowe Ehud Ur Ali Syed Imran 《Cardiovascular diabetology》2006,5(1):1-9