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121.
Pourret Olivier van der Ent Antony Hursthouse Andrew Irawan Dasapta Erwin Liu Haiyan Wiche Oliver 《Plant and Soil》2022,476(1-2):721-728
Plant and Soil - Rare earth elements (REEs) and normalized REE patterns determined in plant and soil samples represent powerful tools to trace biogeochemical processes during weathering, soil... 相似文献
122.
Daniel P. Oehme Matthew T. Downton Monika S. Doblin John Wagner Michael J. Gidley Antony Bacic 《Plant physiology》2015,168(1):3-17
Flooding is detrimental for plants, primarily because of restricted gas exchange underwater, which leads to an energy and carbohydrate deficit. Impeded gas exchange also causes rapid accumulation of the volatile ethylene in all flooded plant cells. Although several internal changes in the plant can signal the flooded status, it is the pervasive and rapid accumulation of ethylene that makes it an early and reliable flooding signal. Not surprisingly, it is a major regulator of several flood-adaptive plant traits. Here, we discuss these major ethylene-mediated traits, their functional relevance, and the recent progress in identifying the molecular and signaling events underlying these traits downstream of ethylene. We also speculate on the role of ethylene in postsubmergence recovery and identify several questions for future investigations.Come gather round people wherever you roamAnd admit that the waters around you have grownAnd accept it that soon you’ll be drenched to the boneIf your time to you is worth savingAnd you’d better start swimming or you’ll sink like a stoneFor the times they are a-changing…THE TIMES THEY ARE A-CHANGIN''Words and Music by Bob DylanCopyright © 1963, 1964 Warner Bros. Inc.Copyright Renewed 1991, 1992 Special Rider MusicInternational Copyright Secured. All Rights Reserved.Reprinted by Permission.Fifty years later, these prophetic words from Dylan’s legendary song strangely ring true. We live in an increasingly wetter world. Flooding events have become more frequent, severe, and unpredictable, a trend that is linked to climate change (Arnell and Liu, 2001; Hirabayashi et al., 2013). Not only do they destroy human lives, but also, they affect plants, on which we depend so much. Flooding negatively affects plant biodiversity, natural species distribution, and global food production because of crop losses (Silvertown et al., 1999; Normile, 2008), because most terrestrial plants, including major crops, are extremely sensitive to wet conditions. It might seem counterintuitive that a molecule so biologically benign and indispensable for plant growth and function is harmful when present in excess. However, this is attributed to the fact that water is an extremely poor medium for gas diffusion. Hampered gas exchange with flooded organs leads to restriction of two vital plant processes: photosynthesis and respiration. The problem is compounded by stagnant and/or turbid floodwaters, because this further restricts the availability of light and oxygen. An energy crisis quickly results owing to an imbalance between energy production and consumption, ultimately causing plant mortality. Flooding survival tactics in the plant kingdom vary widely and include several morphological, anatomical, physiological, and molecular changes that can prolong survival and even facilitate permanent habitation in wet environments (Voesenek and Bailey-Serres, 2015). Initiation of these changes requires accurate and timely perception of water inundation to initiate adaptive responses. The term flooding encompasses both waterlogging and submergence. Waterlogging implies soil flooding, where only roots are exposed to wet conditions. Submergence also immerses the shoot (partially or wholly). Unless otherwise specified, this nomenclature will be used throughout this article. 相似文献
123.
Expression of Ca2+-permeable two-pore channels rescues NAADP signalling in TPC-deficient cells 下载免费PDF全文
Margarida Ruas Lianne C Davis Cheng-Chang Chen Anthony J Morgan Kai-Ting Chuang Timothy F Walseth Christian Grimm Clive Garnham Trevor Powell Nick Platt Frances M Platt Martin Biel Christian Wahl-Schott John Parrington Antony Galione 《The EMBO journal》2015,34(13):1743-1758
The second messenger NAADP triggers Ca2+ release from endo-lysosomes. Although two-pore channels (TPCs) have been proposed to be regulated by NAADP, recent studies have challenged this. By generating the first mouse line with demonstrable absence of both Tpcn1 and Tpcn2 expression (Tpcn1/2−/−), we show that the loss of endogenous TPCs abolished NAADP-dependent Ca2+ responses as assessed by single-cell Ca2+ imaging or patch-clamp of single endo-lysosomes. In contrast, currents stimulated by PI(3,5)P2 were only partially dependent on TPCs. In Tpcn1/2−/− cells, NAADP sensitivity was restored by re-expressing wild-type TPCs, but not by mutant versions with impaired Ca2+-permeability, nor by TRPML1. Another mouse line formerly reported as TPC-null likely expresses truncated TPCs, but we now show that these truncated proteins still support NAADP-induced Ca2+ release. High-affinity [32P]NAADP binding still occurs in Tpcn1/2−/− tissue, suggesting that NAADP regulation is conferred by an accessory protein. Altogether, our data establish TPCs as Ca2+-permeable channels indispensable for NAADP signalling. 相似文献
124.
Rebecca A. Capel Emma L. Bolton Wee K. Lin Daniel Aston Yanwen Wang Wei Liu Xin Wang Rebecca-Ann B. Burton Duncan Bloor-Young Kai-Ting Shade Margarida Ruas John Parrington Grant C. Churchill Ming Lei Antony Galione Derek A. Terrar 《The Journal of biological chemistry》2015,290(50):30087-30098
Ca2+-permeable type 2 two-pore channels (TPC2) are lysosomal proteins required for nicotinic acid adenine dinucleotide phosphate (NAADP)-evoked Ca2+ release in many diverse cell types. Here, we investigate the importance of TPC2 proteins for the physiology and pathophysiology of the heart. NAADP-AM failed to enhance Ca2+ responses in cardiac myocytes from Tpcn2−/− mice, unlike myocytes from wild-type (WT) mice. Ca2+/calmodulin-dependent protein kinase II inhibitors suppressed actions of NAADP in myocytes. Ca2+ transients and contractions accompanying action potentials were increased by isoproterenol in myocytes from WT mice, but these effects of β-adrenoreceptor stimulation were reduced in myocytes from Tpcn2−/− mice. Increases in amplitude of L-type Ca2+ currents evoked by isoproterenol remained unchanged in myocytes from Tpcn2−/− mice showing no loss of β-adrenoceptors or coupling mechanisms. Whole hearts from Tpcn2−/− mice also showed reduced inotropic effects of isoproterenol and a reduced tendency for arrhythmias following acute β-adrenoreceptor stimulation. Hearts from Tpcn2−/− mice chronically exposed to isoproterenol showed less cardiac hypertrophy and increased threshold for arrhythmogenesis compared with WT controls. Electron microscopy showed that lysosomes form close contacts with the sarcoplasmic reticulum (separation ∼25 nm). We propose that Ca2+-signaling nanodomains between lysosomes and sarcoplasmic reticulum dependent on NAADP and TPC2 comprise an important element in β-adrenoreceptor signal transduction in cardiac myocytes. In summary, our observations define a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junctions as unexpected but major contributors in the acute actions of β-adrenergic signaling in the heart and also in stress pathways linking chronic stimulation of β-adrenoceptors to hypertrophy and associated arrhythmias. 相似文献
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128.
Trevor J. C. Beebee John Buckley Ivor Evans Jim P. Foster Antony H. Gent Chris P. Gleed-Owen Geoffrey Kelly Graham Rowe Charles Snell Julia T. Wycherley Inga Zeisset 《Biodiversity and Conservation》2005,14(7):1607-1626
Introduced species often pose serious threats to biodiversity, but occasionally confusion arises as to whether a species really is introduced or is in fact an overlooked native. A recent UK conservation dilemma has centred on the status of the pool frog Rana lessonae. This species has been the subject of documented introductions from central and southern Europe since the early 1800s, the accepted position being that all UK R. lessonae populations are descended from these introductions. However, a closer examination of early UK literature sources, and recent discoveries of isolated, native R. lessonae populations in Sweden and Norway, led some herpetologists to question whether the species was in fact present as a native at some locations prior to the introductions. Research was initiated along four major lines of enquiry: genetic, bioacoustic, archaeozoological and archival. A high degree of convergence among the genetic and bioacoustic investigations demonstrated that the potentially native UK pool frogs were closely related to Scandinavian frogs, thus ruling out introductions from further south as a potential origin. Subfossil evidence of pool frogs was found from ca. 1000 years before present, demonstrating that the species occurred in the UK prior to known introductions. Archival sources produced no historical support for introductions from northern Europe. The postglacial history inferred for these northern populations is consistent with the known climatic and geographical conditions. Taken together, the evidence for the native status of the pool frog is compelling, and furthermore the UK population appears to be part of a distinct northern clade. 相似文献
129.
Insulin hypersensitivity and resistance to streptozotocin-induced diabetes in mice lacking PTEN in adipose tissue 总被引:7,自引:0,他引:7 下载免费PDF全文
Kurlawalla-Martinez C Stiles B Wang Y Devaskar SU Kahn BB Wu H 《Molecular and cellular biology》2005,25(6):2498-2510
In adipose tissue, insulin controls glucose and lipid metabolism through the intracellular mediators phosphatidylinositol 3-kinase and serine-threonine kinase AKT. Phosphatase and a tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of the phosphatidylinositol 3-kinase/AKT pathway, is hypothesized to inhibit the metabolic effects of insulin. Here we report the generation of mice lacking PTEN in adipose tissue. Loss of Pten results in improved systemic glucose tolerance and insulin sensitivity, associated with decreased fasting insulin levels, increased recruitment of the glucose transporter isoform 4 to the cell surface in adipose tissue, and decreased serum resistin levels. Mutant animals also exhibit increased insulin signaling and AMP kinase activity in the liver. Pten mutant mice are resistant to developing streptozotocin-induced diabetes. Adipose-specific Pten deletion, however, does not alter adiposity or plasma fatty acids. Our results demonstrate that in vivo PTEN is a potent negative regulator of insulin signaling and insulin sensitivity in adipose tissue. Furthermore, PTEN may be a promising target for nutritional and/or pharmacological interventions aimed at reversing insulin resistance. 相似文献
130.