bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evolutionary History and Stress Regulation of Plant Receptor-Like Kinase/Pelle Genes
Authors: Lehti-Shiu Melissa D. , Zou Cheng , Hanada Kousuke , Shiu Shin-Han 
Published: March 2009

Abstract
Receptor-Like Kinase (RLK)/Pelle genes play roles ranging from growth regulation to defense response, and the dramatic expansion of this family has been postulated to be crucial for plant-specific adaptations. Despite this, little is known about the history of or the factors that contributed to the dramatic expansion of this gene family. In this study, we show that expansion coincided with the establishment of land plants and that RLK/Pelle subfamilies were established early in land plant evolution. The RLK/Pelle family expanded at a significantly higher rate than other kinases, due in large part to expansion of a few subfamilies by tandem duplication. Interestingly, these subfamilies tend to have members with known roles in defense response, suggesting that their rapid expansion was likely a consequence of adaptation to fast-evolving pathogens. Arabidopsis (Arabidopsis thaliana) expression data support the importance of RLK/Pelles in biotic stress response. We found that hundreds of RLK/Pelles are up-regulated by biotic stress. Furthermore, stress responsiveness is correlated with the degree of tandem duplication in RLK/Pelle subfamilies. Our findings suggest a link between stress response and tandem duplication and provide an explanation for why a large proportion of the RLK/Pelle gene family is found in tandem repeats. In addition, our findings provide a useful framework for potentially predicting RLK/Pelle stress functions based on knowledge of expansion pattern and duplication mechanism. Finally, we propose that the detection of highly variable molecular patterns associated with specific pathogens/parasites is the main reason for the up-regulation of hundreds of RLK/Pelles under biotic stress.
Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis
Authors: Brewer Philip B. , Dun Elizabeth A. , Ferguson Brett J. , Rameau Catherine , Beveridge Christine A. 
Published: March 2009

Abstract
During the last century, two key hypotheses have been proposed to explain apical dominance in plants: auxin promotes the production of a second messenger that moves up into buds to repress their outgrowth, and auxin saturation in the stem inhibits auxin transport from buds, thereby inhibiting bud outgrowth. The recent discovery of strigolactone as the novel shoot-branching inhibitor allowed us to test its mode of action in relation to these hypotheses. We found that exogenously applied strigolactone inhibited bud outgrowth in pea (Pisum sativum) even when auxin was depleted after decapitation. We also found that strigolactone application reduced branching in Arabidopsis (Arabidopsis thaliana) auxin response mutants, suggesting that auxin may act through strigolactones to facilitate apical dominance. Moreover, strigolactone application to tiny buds of mutant or decapitated pea plants rapidly stopped outgrowth, in contrast to applying N-1-naphthylphthalamic acid (NPA), an auxin transport inhibitor, which significantly slowed growth only after several days. Whereas strigolactone or NPA applied to growing buds reduced bud length, only NPA blocked auxin transport in the bud. Wild-type and strigolactone biosynthesis mutant pea and Arabidopsis shoots were capable of instantly transporting additional amounts of auxin in excess of endogenous levels, contrary to predictions of auxin transport models. These data suggest that strigolactone does not act primarily by affecting auxin transport from buds. Rather, the primary repressor of bud outgrowth appears to be the auxin-dependent production of strigolactones.
Studies ofaberrant phyllotaxy1Mutants of Maize Indicate Complex Interactions between Auxin and Cytokinin Signaling in the Shoot Apical Meristem
Authors: Lee Byeong-ha , Johnston Robyn , Yang Yan , Gallavotti Andrea , Kojima Mikiko , Travençolo Bruno A.N. , Costa Luciano da F. , Sakakibara Hitoshi , Jackson David 
Published: March 2009

AbstractOne of the most fascinating aspects of plant morphology is the regular geometric arrangement of leaves and flowers, called phyllotaxy. The shoot apical meristem (SAM) determines these patterns, which vary depending on species and developmental stage. Auxin acts as an instructive signal in leaf initiation, and its transport has been implicated in phyllotaxy regulation in Arabidopsis (Arabidopsis thaliana). Altered phyllotactic patterns are observed in a maize (Zea mays) mutant, aberrant phyllotaxy1 (abph1, also known as abphyl1), and ABPH1 encodes a cytokinin-inducible type A response regulator, suggesting that cytokinin signals are also involved in the mechanism by which phyllotactic patterns are established. Therefore, we investigated the interaction between auxin and cytokinin signaling in phyllotaxy. Treatment of maize shoots with a polar auxin transport inhibitor, 1-naphthylphthalamic acid, strongly reduced ABPH1 expression, suggesting that auxin or its polar transport is required for ABPH1 expression. Immunolocalization of the PINFORMED1 (PIN1) polar auxin transporter revealed that PIN1 expression marks leaf primordia in maize, similarly to Arabidopsis. Interestingly, maize PIN1 expression at the incipient leaf primordium was greatly reduced in abph1 mutants. Consistently, auxin levels were reduced in abph1, and the maize PIN1 homolog was induced not only by auxin but also by cytokinin treatments. Our results indicate distinct roles for ABPH1 as a negative regulator of SAM size and a positive regulator of PIN1 expression. These studies highlight a complex interaction between auxin and cytokinin signaling in the specification of phyllotactic patterns and suggest an alternative model for the generation of altered phyllotactic patterns in abph1 mutants. We propose that reduced auxin levels and PIN1 expression in abph1 mutant SAMs delay leaf initiation, contributing to the enlarged SAM and altered phyllotaxy of these mutants.
A Signaling Pathway Linking Nitric Oxide Production to Heterotrimeric G Protein and Hydrogen Peroxide Regulates Extracellular Calmodulin Induction of Stomatal Closure in Arabidopsis
Authors: Li Jian-Hua , Liu Yin-Qian , Lü Pin , Lin Hai-Fei , Bai Yang , Wang Xue-Chen , Chen Yu-Ling 
Published: March 2009

AbstractExtracellular calmodulin (ExtCaM) regulates stomatal movement by eliciting a cascade of intracellular signaling events including heterotrimeric G protein, hydrogen peroxide (H2O2), and Ca2+. However, the ExtCaM-mediated guard cell signaling pathway remains poorly understood. In this report, we show that Arabidopsis (Arabidopsis thaliana) NITRIC OXIDE ASSOCIATED1 (AtNOA1)-dependent nitric oxide (NO) accumulation plays a crucial role in ExtCaM-induced stomatal closure. ExtCaM triggered a significant increase in NO levels associated with stomatal closure in the wild type, but both effects were abolished in the Atnoa1 mutant. Furthermore, we found that ExtCaM-mediated NO generation is regulated by GPA1, the Gα-subunit of heterotrimeric G protein. The ExtCaM-dependent NO accumulation was nullified in gpa1 knockout mutants but enhanced by overexpression of a constitutively active form of GPA1 (cGα). In addition, cGα Atnoa1 and gpa1-2 Atnoa1 double mutants exhibited a similar response as did Atnoa1. The defect in gpa1 was rescued by overexpression of AtNOA1. Finally, we demonstrated that G protein activation of NO production depends on H2O2. Reduced H2O2 levels in guard cells blocked the stomatal response of cGα lines, whereas exogenously applied H2O2 rescued the defect in ExtCaM-mediated stomatal closure in gpa1 mutants. Moreover, the atrbohD/F mutant, which lacks the NADPH oxidase activity in guard cells, had impaired NO generation in response to ExtCaM, and H2O2-induced stomatal closure and NO accumulation were greatly impaired in Atnoa1. These findings have established a signaling pathway leading to ExtCaM-induced stomatal closure, which involves GPA1-dependent activation of H2O2 production and subsequent AtNOA1-dependent NO accumulation.
Disruption of Glycosylphosphatidylinositol-Anchored Lipid Transfer Protein Gene Altered Cuticular Lipid Composition, Increased Plastoglobules, and Enhanced Susceptibility to Infection by the Fungal Pathogen Alternaria brassicicola
Authors: Lee Saet Buyl , Go Young Sam , Bae Hyun-Jong , Park Jong Ho , Cho Sung Ho , Cho Hong Joo , Lee Dong Sook , Park Ohkmae K. , Hwang Inhwan , Suh Mi Chung 
Published: March 2009

Abstract
All aerial parts of vascular plants are covered with cuticular waxes, which are synthesized by extensive export of intracellular lipids from epidermal cells to the surface. Although it has been suggested that plant lipid transfer proteins (LTPs) are involved in cuticular lipid transport, the in planta evidence is still not clear. In this study, a glycosylphosphatidylinositol-anchored LTP (LTPG1) showing higher expression in epidermal peels of stems than in stems was identified from an Arabidopsis (Arabidopsis thaliana) genome-wide microarray analysis. The expression of LTPG1 was observed in various tissues, including the epidermis, stem cortex, vascular bundles, mesophyll cells, root tips, pollen, and early-developing seeds. LTPG1 was found to be localized in the plasma membrane. Disruption of the LTPG1 gene caused alterations of cuticular lipid composition, but no significant changes on total wax and cutin monomer loads were seen. The largest reduction (10 mass %) in the ltpg1 mutant was observed in the C29 alkane, which is the major component of cuticular waxes in the stems and siliques. The reduced content was overcome by increases of the C29 secondary alcohols and C29 ketone wax loads. The ultrastructure analysis of ltpg1 showed a more diffuse cuticular layer structure, protrusions of the cytoplasm into the vacuole in the epidermis, and an increase of plastoglobules in the stem cortex and leaf mesophyll cells. Furthermore, the ltpg1 mutant was more susceptible to infection by the fungus Alternaria brassicicola than the wild type. Taken together, these results indicated that LTPG1 contributed either directly or indirectly to cuticular lipid accumulation.
High expression of Pirh2, an E3 ligase for p27, is associated with low expression of p27 and poor prognosis in head and neck cancers
Authors: Shimada Mai , Kitagawa Kyoko , Dobashi Yoh , Isobe Tomoyasu , Hattori Takayuki , Uchida Chiharu , Abe Kenji , Kotake Yojiro , Oda Toshiaki , Suzuki Hiroyuki , Hashimoto Kenji , Kitagawa Masatoshi 
Published: March 2009

Downregulation of the cyclin‐dependent kinase inhibitory protein p27 is frequently observed in various cancers due to enhancement of its degradation. We recently reported that p53‐inducible protein with RING‐H2 domain (Pirh2) is a novel ubiquitin ligase for p27, required for the ubiquitylation and consequent degradation of p27 protein. However, there is no reports about the involvement of Pirh2 in both p27 downregulation and pathogenesis in human cancers. In the present study, we investigated them using cultured cell lines and surgical specimens derived from human head and neck squamous cell carcinoma (HNSCC). Depletion of Pirh2 by short interfering RNA induced accumulation of p27 and inhibited the growth of cultured HNSCC cells. By immunohistochemical analysis in 57 cases of HNSCC specimens, higher levels of Pirh2 expression (labeling index ≥ 60%) were found in 61.4% of HNSCC in comparison with 0% of normal mucosa. In addition, 83.3% of HNSCC with lower p27 expression (labeling index < 20%) displayed high Pirh2 levels. Therefore, Pirh2 expression was inversely correlated with p27 expression. Finally, Pirh2 expression was well correlated with poor prognosis. These findings suggest that Pirh2 overexpression may have an important role in the development and maintenance of HNSCC at least partially through p27 degradation, and that Pirh2 may be a potential molecular target for human HNSCC. (Cancer Sci 2009; 100: 866–872)
Genesis of an over‐thickened shoreface sandstone tongue: The Rannoch and Etive formations of the Middle Jurassic Brent delta, North Sea
Authors: Helle K. , Helland‐Hansen W. 
Published: March 2009

ABSTRACTProgradational, wave‐dominated shoreface sandstones are typically reported to have thicknesses of less than 30 m. The shoreface sandstones of the Rannoch and Etive formations in the North Sea Brent Group, however, comprise far greater thicknesses (in places exceeding 100 m). The genesis of these successions have not been well understood, and the purpose of this study is to investigate within the framework of facies geometries in both modern and ancient depositional systems how the Rannoch‐Etive sandstones could have been formed, on a local‐regional scale.The facies analysis concludes that the Brent delta advance represents a single progradational event, not punctuated by transgressions. In such a scenario, the vertical sandstone thickness would be determined by: 1) shoreline trajectory angle, 2) the horizontal (dip‐directed) length of shoreface sand (typically 1–2 km in modern systems), and 3) shoreface sand pinch‐out depth (typically 5–12 m in modern systems). Within a framework of modern facies geometries, a 100 m thick vertical shoreface sandstone succession could result from a regression characterised by a shoreline trajectory of 2.6–5.4° (implying 80–95 m rise in relative sea level per 1–2 km of progradation), a 5–12 m deep shoreface sand pinch‐out depth, and a 1–2 km shoreface sand length.If, however, one applies such a model for the entire Brent delta progradation in the study area (200 km) this implies a rise in relative sea level of c. 5000 m, which clearly would be associated with large amounts of deposits accumulating behind and in front of the advancing shoreline. Such deposits are not present, which implies that modern facies geometries do not apply and that rising sea level was not of major importance in defining stratigraphic architecture. It is more likely that the regional overthickening of the Rannoch‐Etive sandstones resulted from progradation with a deep shoreface sand pinch‐out depth.
Prognostic factor analysis of the survival of elderly patients with AML in the MRC AML11 and LRF AML14 trials
Authors: Wheatley Keith , Brookes Cassandra L. , Howman Andrew J. , Goldstone Anthony H. , Milligan Donald W. , Prentice Archibald G. , Moorman Anthony V. , Burnett Alan K. ,   on behalf of the United Kingdom National Cancer Research Institute Haematological Oncology Clinical Studies Group and Acute Myeloid Leukaemia Subgroup
Published: March 2009

SummaryThis analysis, of 2483 patients with acute myeloid leukaemia (AML) aged 60+ years entered into two UK trials, was performed to determine the baseline parameters related to survival and to develop a risk index. The Medical Research Council (MRC) AML11 trial (n = 1071) was used to develop the index; this was validated using data from the Leukaemia Research fund (LRF) AML14 trial on 1137 intensively (AML14I) and 275 non‐intensively (AML14NI) treated patients. In AML11, cytogenetic group, age, white blood count, performance status and type of AML (de novo, secondary) were all highly significantly related to prognosis in multivariate analysis. The regression coefficients were used to define good, standard and poor risk groups, with 1‐year survival of 53%, 43% and 16% respectively (P < 0·0001). The risk index showed very good discrimination in both AML14I and AML14NI (both P < 0·0001), thereby providing validation, although survival in all groups was very poor in AML14NI. The risk factors for survival in older AML patients were similar to those in younger ones and discrimination of patient groups with relatively good to very poor prognosis was possible. These risk groups apply to both intensively and non‐intensively treated patients. Randomized trials of intensive versus non‐intensive therapy are needed to determine which types of patient should be given which type of treatment.
Prior rituximab correlates with less acute graft‐versus‐host disease and better survival in B‐cell lymphoma patients who received allogeneic peripheral blood stem cell transplantation
Authors: Ratanatharathorn Voravit , Logan Brent , Wang Dan , Horowitz Mary , Uberti Joseph P. , Ringden Olle , Gale Robert Peter , Khoury Hanna , Arora Mukta , Spellman Stephen , Cutler Corey , Antin Joseph , Bornhaüser Martin , Hale Gregory , Verdonck Leo , Cairo Mitchell , Gupta Vikas , Pavletic Steven ,   for the Center for International Blood and Marrow Transplant Research (CIBMTR), Milwaukee, WI, USA
Published: March 2009

SummaryPrior therapy with rituximab might attenuate disparate histocompatibility antigen presentation by B cells, thus decreased the risk of acute graft‐versus‐host disease (GVHD) and improved survival. We tested this hypothesis by comparing the outcomes of 435 B‐cell lymphoma patients who received allogeneic transplantation from 1999 to 2004 in the Center for International Blood and Marrow Transplant Research database: 179 subjects who received rituximab within 6 months prior to transplantation (RTX cohort) and 256 subjects who did not receive RTX within 6 months prior to transplantation (No‐RTX cohort). The RTX cohort had a significantly lower incidence of treatment‐related mortality (TRM) [relative risk (RR) = 0·68; 95% confidence interval (CI), 0·47–1·0; P = 0·05], lower acute grade II–IV (RR = 0·72; 95% CI, 0·53–0·97; P = 0·03) and III–IV GVHD (RR = 0·55; 95% CI, 0·34–0·91; P = 0·02). There was no difference in the risk of chronic GVHD, disease progression or relapse. Progression‐free survival (PFS) (RR = 0·68; 95% CI 0·50–0·92; P = 0·01) and overall survival (OS) (RR = 0·63; 95% CI, 0·46–0·86; P = 0·004) were significantly better in the RTX cohort. Prior RTX therapy correlated with less acute GVHD, similar chronic GVHD, less TRM, better PFS and OS.
Climate change and cyclic predator–prey population dynamics in the high Arctic
Authors: GILG OLIVIER , SITTLER BENOÎT , HANSKI ILKKA 
Published: March 2009

AbstractThe high Arctic has the world's simplest terrestrial vertebrate predator–prey community, with the collared lemming being the single main prey of four predators, the snowy owl, the Arctic fox, the long‐tailed skua, and the stoat. Using a 20‐year‐long time series of population densities for the five species and a dynamic model that has been previously parameterized for northeast Greenland, we analyzed the population and community level consequences of the ongoing and predicted climate change. Species' responses to climate change are complex, because in addition to the direct effects of climate change, which vary depending on species' life histories, species are also affected indirectly due to, e.g., predator–prey interactions. The lemming–predator community exemplifies these complications, yet a robust conclusion emerges from our modeling: in practically all likely scenarios of how climate change may influence the demography of the species, climate change increases the length of the lemming population cycle and decreases the maximum population densities. The latter change in particular is detrimental to the populations of the predators, which are adapted to make use of the years of the greatest prey abundance. Therefore, climate change will indirectly reduce the predators' reproductive success and population densities, and may ultimately lead to local extinction of some of the predator species. Based on these results, we conclude that the recent anomalous observations about lack of cyclic lemming dynamics in eastern Greenland may well be the first signs of a severe impact of climate change on the lemming–predator communities in Greenland and elsewhere in the high Arctic.
Response of carbon fluxes to drought in a coastal plain loblolly pine forest
Authors: NOORMETS ASKO , GAVAZZI MICHAEL J. , MCNULTY STEVE G. , DOMEC JEAN‐CHRISTOPHE , SUN GE , KING JOHN S. , CHEN JIQUAN 
Published: March 2009

AbstractFull accounting of ecosystem carbon (C) pools and fluxes in coastal plain ecosystems remains less studied compared with upland systems, even though the C stocks in these systems may be up to an order of magnitude higher, making them a potentially important component in regional C cycle. Here, we report C pools and CO2 exchange rates during three hydrologically contrasting years (i.e. 2005–2007) in a coastal plain loblolly pine plantation in North Carolina, USA. The daily temperatures were similar among the study years and to the long‐term (1971–2000) average, whereas the amount and timing of precipitation differed significantly. Precipitation was the largest in 2005 (147 mm above normal), intermediate in 2006 (48 mm below) and lowest in 2007 (486 mm below normal). The forest was a strong C sink during all years, sequestering 361 ± 67 (2005), 835 ± 55 (2006) and 724 ± 55 (2007) g C m−2 yr−1 according to eddy covariance measurements of net ecosystem CO2 exchange (NEE). The interannual differences in NEE were traced to drought‐induced declines in canopy and whole tree hydraulic conductances, which declined with growing precipitation deficit and decreasing soil volumetric water content (VWC). In contrast, the interannual differences were small in gross ecosystem productivity (GEP) and ecosystem respiration (ER), both seemingly insensitive to drought. However, the drought sensitivity of GEP was masked by higher leaf area index and higher photosynthetically active radiation during the dry year. Normalizing GEP by these factors enhanced interannual differences, but there were no signs of suppressed GEP at low VWC during any given year. Although ER was very consistent across the 3 years, and not suppressed by low VWC, the total respiratory cost as a fraction of net primary production increased with annual precipitation and the contribution of heterotrophic respiration (Rh) was significantly higher during the wettest year, exceeding new litter inputs by 58%. Although the difference was smaller during the other 2 years (Rh : litterfall ratio was 1.05 in 2006 and 1.10 in 2007), the soils lost about 109 g C m−2 yr−1, outlining their potential vulnerability to decomposition, and pointing to potential management considerations to protect existing soil C stocks.
Quantifying the metabolic cost to an Antarctic liverwort of responding to an abrupt increase in UVB radiation exposure
Authors: SNELL K. R. S. , KOKUBUN T. , GRIFFITHS H. , CONVEY P. , HODGSON D. A. , NEWSHAM K. K. 
Published: March 2009

AbstractWe quantified the metabolic cost to the Antarctic leafy liverwort Cephaloziella varians of responding to an abrupt increase in ultraviolet B (UVB) radiation exposure in the natural environment at Rothera Point on the western Antarctic Peninsula (67 °34′S, 68 °07′W). The liverwort was protected from exposure to UVB radiation for 44 days with screens containing Mylar polyester, after which time its thalli, which are normally black in colour, had become green owing to reduced concentrations of an anthocyanidin, identified here as riccionidin A, in thallus tips. Thalli were then exposed to an abrupt increase in UVB radiation by removing the screens. The thalli became visibly darker within 48 h of the screens being removed, resynthesizing riccionidin A to the same concentration as that present in thalli outside screens during this period. Chlorophyll fluorescence measurements indicated that nonphotochemical quenching was higher in the thalli formerly under the screens than in those not previously covered with screens, but that Fv/Fm and photochemical quenching were the same in the two groups of thalli. We used data from aqueous phase oxygen electrode measurements to calculate an estimate for carbon fixation by C. varians during the 48 h after the screens were removed. Assuming a photosynthetic quotient for Antarctic bryophytes of 1, these analyses indicated that the minimum weight of carbon used to synthesize riccionidin A was equivalent to 1.85% of the carbon fixed by thalli during the 48 h after the abrupt increase in UVB radiation exposure.