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"Gray, William"
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Ansel Adams : the Grand Canyon and the Southwest
\"Next to Yosemite and the High Sierra, the Southwest was closest to Ansel Adams' heart. It was here, in the early 1930's, that he was inspired to make photography his life's work. He would return to the region again and again. In his words, \"wherever one goes in the Southwest one encounters magic, strength, and beauty.\" Today the Grand Canyon is one of America's most popular national parks, hosting more than six million visitors each year. This special edition paperback reproduces Ansel Adams' exquisite photographs of the Canyon alongside iconic images of the Southwest, spanning Arizona, California, Colorado, New Mexico, Texas, and Utah. This collection of seventy duotone photographs is complemented by Adams' vivid writings about his travels in the region.\"--Back cover.
BOOK
A subset of plasma membrane-localized PP2C.D phosphatases negatively regulate SAUR-mediated cell expansion in Arabidopsis
The plant hormone auxin regulates numerous growth and developmental processes throughout the plant life cycle. One major function of auxin in plant growth and development is the regulation of cell expansion. Our previous studies have shown that SMALL AUXIN UP RNA (SAUR) proteins promote auxin-induced cell expansion via an acid growth mechanism. These proteins inhibit the PP2C.D family phosphatases to activate plasma membrane (PM) H+-ATPases and thereby promote cell expansion. However, the functions of individual PP2C.D phosphatases are poorly understood. Here, we investigated PP2C.D-mediated control of cell expansion and other aspects of plant growth and development. The nine PP2C.D family members exhibit distinct subcellular localization patterns. Our genetic findings demonstrate that the three plasma membrane-localized members, PP2C.D2, PP2C.D5, and PP2C.D6, are the major regulators of cell expansion. These phosphatases physically interact with SAUR19 and PM H+-ATPases, and inhibit cell expansion by dephosphorylating the penultimate threonine of PM H+-ATPases. PP2C.D genes are broadly expressed and are crucial for diverse plant growth and developmental processes, including apical hook development, phototropism, and organ growth. GFP-SAUR19 overexpression suppresses the growth defects conferred by PP2C.D5 overexpression, indicating that SAUR proteins antagonize the growth inhibition conferred by the plasma membrane-localized PP2C.D phosphatases. Auxin and high temperature upregulate the expression of some PP2C.D family members, which may provide an additional layer of regulation to prevent plant overgrowth. Our findings provide novel insights into auxin-induced cell expansion, and provide crucial loss-of-function genetic support for SAUR-PP2C.D regulatory modules controlling key aspects of plant growth.
Journal Article
Essentials of multiphase flow and transport in porous media
Learn the fundamental concepts that underlie the physics of multiphase flow and transport in porous media with the information in Essentials of Multiphase Flow in Porous Media, which demonstrates the mathematical-physical ways to express and address multiphase flow problems. Find a logical, step-by-step introduction to everything from the simple concepts to the advanced equations useful for addressing real-world problems like infiltration, groundwater contamination, and movement of non-aqueous phase liquids. Discover and apply the governing equations for application to these and other problems in light of the physics that influence system behavior.
eBook
BRASSINOSTEROID-SIGNALING KINASE 3, a plasma membrane-associated scaffold protein involved in early brassinosteroid signaling
Brassinosteroids (BRs) are steroid hormones essential for plant growth and development. The BR signaling pathway has been studied in some detail, however, the functions of the BRASSINOSTEROID-SIGNALING KINASE (BSK) family proteins in the pathway have remained elusive. Through forward genetics, we identified five semi-dominant mutations in the BSK3 gene causing BSK3 loss-of-function and decreased BR responses. We therefore investigated the function of BSK3, a receptor-like cytoplasmic kinase, in BR signaling and plant growth and development. We find that BSK3 is anchored to the plasma membrane via N-myristoylation, which is required for its function in BR signaling. The N-terminal kinase domain is crucial for BSK3 function, and the C-terminal three tandem TPR motifs contribute to BSK3/BSK3 homodimer and BSK3/BSK1 heterodimer formation. Interestingly, the effects of BSK3 on BR responses are dose-dependent, depending on its protein levels. Our genetic studies indicate that kinase dead BSK3K86R protein partially rescues the bsk3-1 mutant phenotypes. BSK3 directly interacts with the BSK family proteins (BSK3 and BSK1), BRI1 receptor kinase, BSU1 phosphatase, and BIN2 kinase. BIN2 phosphorylation of BSK3 enhances BSK3/BSK3 homodimer and BSK3/BSK1 heterodimer formation, BSK3/BRI1 interaction, and BSK3/BSU1 interaction. Furthermore, we find that BSK3 upregulates BSU1 transcript and protein levels to activate BR signaling. BSK3 is broadly expressed and plays an important role in BR-mediated root growth, shoot growth, and organ separation. Together, our findings suggest that BSK3 may function as a scaffold protein to regulate BR signaling. The results of our studies provide new insights into early BR signaling mechanisms.
Journal Article
TMK-based cell-surface auxin signalling activates cell-wall acidification
The phytohormone auxin controls many processes in plants, at least in part through its regulation of cell expansion
1
. The acid growth hypothesis has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism that underlies auxin-induced cell-wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane H
+
-ATPase that pumps protons into the apoplast
2
, yet how auxin activates its phosphorylation remains unclear. Here we show that the transmembrane kinase (TMK) auxin-signalling proteins interact with plasma membrane H
+
-ATPases, inducing their phosphorylation, and thereby promoting cell-wall acidification and hypocotyl cell elongation in
Arabidopsis
. Auxin induced interactions between TMKs and H
+
-ATPases in the plasma membrane within seconds, as well as TMK-dependent phosphorylation of the penultimate threonine residue on the H+-ATPases. Our genetic, biochemical and molecular evidence demonstrates that TMKs directly phosphorylate plasma membrane H
+
-ATPase and are required for auxin-induced H
+
-ATPase activation, apoplastic acidification and cell expansion. Thus, our findings reveal a crucial connection between auxin and plasma membrane H
+
-ATPase activation in regulating apoplastic pH changes and cell expansion through TMK-based cell surface auxin signalling.
Auxin induces transmembrane-kinase-dependent activation of H
+
-ATPase in the plasma membrane through phosphorylation of its penultimate threonine residue, promoting apoplastic acidification and hypocotyl cell elongation in
Arabidopsis
.
Journal Article
Cell surface and intracellular auxin signalling for H+ fluxes in root growth
Growth regulation tailors development in plants to their environment. A prominent example of this is the response to gravity, in which shoots bend up and roots bend down
1
. This paradox is based on opposite effects of the phytohormone auxin, which promotes cell expansion in shoots while inhibiting it in roots via a yet unknown cellular mechanism
2
. Here, by combining microfluidics, live imaging, genetic engineering and phosphoproteomics in
Arabidopsis thaliana
, we advance understanding of how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on rapid regulation of apoplastic pH, a causative determinant of growth. Cell surface-based TRANSMEMBRANE KINASE1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H
+
-ATPases for apoplast acidification, while intracellular canonical auxin signalling promotes net cellular H
+
influx, causing apoplast alkalinization. Simultaneous activation of these two counteracting mechanisms poises roots for rapid, fine-tuned growth modulation in navigating complex soil environments.
Auxin rapidly modulates root growth through simultaneous activation of two opposing mechanisms—TMK1-mediated apoplast acidification and TIR1/AFB-mediated apoplast alkalinization.
Journal Article
Oxygen isotope constraints on the ventilation of the modern and glacial Pacific
Changes in Pacific tracer reservoirs and transports are thought to be central to the regulation of atmospheric CO
2
on glacial–interglacial timescales. However, there are currently two contrasting views of the circulation of the modern Pacific; the classical view sees southern sourced abyssal waters upwelling to about 1.5 km depth before flowing southward, whereas the bathymetrically constrained view sees the mid-depths (1–2.5 km) largely isolated from the global overturning circulation and predominantly ventilated by diffusion. Furthermore, changes in the circulation of the Pacific under differing climate states remain poorly understood. Through both a modern and a Last Glacial Maximum (LGM) analysis focusing on oxygen isotopes in seawater and benthic foraminifera as conservative tracers, we show that isopycnal diffusion strongly influences the mid-depths of the Pacific. Diapycnal diffusion is most prominent in the subarctic Pacific, where an important return path of abyssal tracers to the surface is identified in the modern state. At the LGM we infer an expansion of North Pacific Intermediate Water, as well as increased layering of the deeper North Pacific which would weaken the return path of abyssal tracers. These proposed changes imply a likely increase in ocean carbon storage within the deep Pacific during the LGM relative to the Holocene.
Journal Article
Mortality in randomised controlled trials using paclitaxel-coated devices for femoropopliteal interventional procedures: an updated patient-level meta-analysis
Numerous randomised clinical trials and real-world studies have supported the safety of paclitaxel-coated devices for the treatment of femoropopliteal occlusive disease. However, a 2018 summary-level meta-analysis suggested an increased mortality risk for paclitaxel-coated devices compared with uncoated control devices. This study presents an updated analysis of deaths using the most complete and current data available from pivotal trials of paclitaxel-coated versus control devices.
Ten trials comparing paclitaxel-coated versus control devices were included in a patient-level pooled analysis. Cox regression models were used to evaluate the effect of paclitaxel exposure on risk of death in both intention-to-treat (ITT; primary analysis) and three as-treated analysis sets accounting for treatment group crossover at the index procedure and over time. The effect of paclitaxel dose and baseline covariates were also evaluated.
A total of 2666 participants were included with a median follow-up of 4·9 years. No significant increase in deaths was observed for patients treated with paclitaxel-coated devices. This was true in the ITT analysis (hazard ratio [HR] 1·14, 95% CI 0·93–1·40), the as-treated analysis (HR 1·13, 95% CI 0·92–1·39), and in two crossover analyses: 1·07 (0·87–1·31) when late crossovers were censored and 1·04 (0·84–1·28) when crossovers were analysed from the date of paclitaxel exposure. There was no significant effect of paclitaxel dose on mortality risk.
This meta-analysis found no association between paclitaxel-coated device exposure and risk of death, providing reassurance to patients, physicians, and regulators on the safety of paclitaxel-coated devices.
Becton Dickinson, Boston Scientific, Cook, Medtronic, Philips, Surmodics, and TriReme Medical.
Journal Article