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91.
A. Martijn Antheunisse Roos Loeb Marzia Miletto Leon P. M. Lamers Hendrikus J. Laanbroek Jos T. A. Verhoeven 《Plant and Soil》2007,292(1-2):45-61
In the framework of rehabilitation efforts to enhance the ecological value of closed-off estuaries, we studied the effects
of restoring a tidal movement and seawater incursion on soil nitrogen conversion rates and vegetation response of semi-natural
and agricultural grasslands in an outdoor mesocosm experiment. Intact soil monoliths including vegetation were collected in
June 2004 on two locations on the shores of the Haringvliet lagoon in the south-western part of the Netherlands, which used
to be a well-developed estuary before closure in 1970. For more than 1 year, soil monoliths were continuously subjected to
a full-factorial combination of tidal treatment [stagnant/tidal (0.20 m amplitude)] and water type [(freshwater, oligohaline
(salinity = 3)]. Soil, soil moisture and water nitrogen concentrations were monitored for a year, as well as vegetation response
and nitrogen conversion rates in the soil. As expected, nitrogen mineralization rates were enhanced by the tidal treatment
in comparison with the stagnant treatment. Denitrification rates however, were much less affected by tide and were even lower
in the tidal treatments after 3 months in the agricultural grassland soils, implying that in general, soils were more oxic
in the tidal treatments. Oligohaline treatments had virtually no effect on soil nitrogen conversion rates compared to freshwater
treatments. Vegetation performance, however, was lower under saline conditions, especially in the semi-natural grassland.
No further significant differences in response to the tidal and oligohaline treatments were found between the two soils although
they differed strongly in soil characteristics. We conclude that if the rehabilitation measures in the former Haringvliet
estuary are carried out as planned, drastic changes in soil nitrogen processes and vegetation composition will not occur. 相似文献
92.
93.
In most species, some individuals delay reproduction or occupy inferior breeding positions. The queue hypothesis tries to explain both patterns by proposing that individuals strategically delay breeding (queue) to acquire better breeding or social positions. In 1995, Ens, Weissing, and Drent addressed evolutionarily stable queuing strategies in situations with habitat heterogeneity. However, their model did not consider the non-mutually exclusive individual quality hypothesis, which suggests that some individuals delay breeding or occupy inferior breeding positions because they are poor competitors. Here we extend their model with individual differences in competitive abilities, which are probably plentiful in nature. We show that including even the smallest competitive asymmetries will result in individuals using queuing strategies completely different from those in models that assume equal competitors. Subsequently, we investigate how well our models can explain settlement patterns in the wild, using a long-term study on oystercatchers. This long-lived shorebird exhibits strong variation in age of first reproduction and territory quality. We show that only models that include competitive asymmetries can explain why oystercatchers' settlement patterns depend on natal origin. We conclude that predictions from queuing models are very sensitive to assumptions about competitive asymmetries, while detecting such differences in the wild is often problematic. 相似文献
94.
In the fungal kingdom, the ability to cause disease in plants appears to have arisen multiple times during evolution. In many cases, the ability to infect particular plant species depends on specific genes that distinguish virulent fungi from their sometimes closely related nonvirulent relatives. These genes encode host-determining "virulence factors," including small, secreted proteins and enzymes involved in the synthesis of toxins. These virulence factors typically are involved in evolutionary arms races between plants and pathogens. We briefly summarize current knowledge of these virulence factors from several fungal species in terms of function, phylogenetic distribution, sequence variation, and genomic location. Second, we address some issues that are relevant to the evolution of virulence in fungi toward plants; in particular, horizontal gene transfer and the genomic organization of virulence genes. 相似文献
95.
van Donselaar E Posthuma G Zeuschner D Humbel BM Slot JW 《Traffic (Copenhagen, Denmark)》2007,8(5):471-485
Immunogold labeling of cryosections according to Tokuyasu (Tokuyasu KT. A technique for ultracyotomy of cell suspensions and tissues. J Cell Biol 1973;57:551–565), is an important and widely used method for immunoelectron microscopy. These sections are cut from material that is chemically fixed at room temperature (room temparature fixation, RTF). Lately in many morphological studies fast freezing followed by cryosubstitution fixation (CSF) is used instead of RTF. We have explored some new methods for applying immunogold labeling on cryosections from high‐pressure frozen cells (HepG2 cells, primary chondrocytes) and tissues (cartilage and exocrine pancreas). As immunolabeling has to be carried out on thawed and stable sections, we explored two ways to achieve this: (1) The section fixation method, as briefly reported before (Liou W et al. Histochem Cell Biol 1996;106:41–58 and Möbius W et al. J Histochem Cytochem 2002;50:43–55.) in which cryosections from freshly frozen cells were stabilized in mixtures of sucrose and methyl cellulose and varying concentrations of glutaraldehyde, formaldehyde and uranyl acetate (UA). Only occasionally does this method reveal section areas with excellent cell preservation and negatively stained membranes like Tokuyasu sections of RTF material. (Liou et al.) (2) The rehydration method, a novel approach, in which CSF with glutaraldehyde and/or osmium tetroxide (OsO4) was followed by rehydration and cryosectioning as in the Tokuyasu method. Especially, the addition of UA and low concentrations of water to the CSF medium favored superb membrane contrast. Immunogold labeling was as efficient as with the Tokuyasu method. 相似文献
96.
Joanna K. Polko Jop A. van Rooij Steffen Vanneste Ronald Pierik Ankie M.H. Ammerlaan Marleen H. Vergeer-van Eijk Fionn McLoughlin Kerstin Gühl Gert Van Isterdael Laurentius A.C.J. Voesenek Frank F. Millenaar Tom Beeckman Anton J.M. Peeters Athanasius F.M. Marée Martijn van Zanten 《Plant physiology》2015,169(1):194-208
97.
Dimitris Typas Martijn S. Luijsterburg Wouter W. Wiegant Michaela Diakatou Angela Helfricht Peter E. Thijssen Bram van?de?Broek Leon H. Mullenders Haico van?Attikum 《Nucleic acids research》2015,43(14):6919-6933
The faithful repair of DNA double-strand breaks (DSBs) is essential to safeguard genome stability. DSBs elicit a signaling cascade involving the E3 ubiquitin ligases RNF8/RNF168 and the ubiquitin-dependent assembly of the BRCA1-Abraxas-RAP80-MERIT40 complex. The association of BRCA1 with ubiquitin conjugates through RAP80 is known to be inhibitory to DSB repair by homologous recombination (HR). However, the precise regulation of this mechanism remains poorly understood. Through genetic screens we identified USP26 and USP37 as key de-ubiquitylating enzymes (DUBs) that limit the repressive impact of RNF8/RNF168 on HR. Both DUBs are recruited to DSBs where they actively remove RNF168-induced ubiquitin conjugates. Depletion of USP26 or USP37 disrupts the execution of HR and this effect is alleviated by the simultaneous depletion of RAP80. We demonstrate that USP26 and USP37 prevent excessive spreading of RAP80-BRCA1 from DSBs. On the other hand, we also found that USP26 and USP37 promote the efficient association of BRCA1 with PALB2. This suggests that these DUBs limit the ubiquitin-dependent sequestration of BRCA1 via the BRCA1-Abraxas-RAP80-MERIT40 complex, while promoting complex formation and cooperation of BRCA1 with PALB2-BRCA2-RAD51 during HR. These findings reveal a novel ubiquitin-dependent mechanism that regulates distinct BRCA1-containing complexes for efficient repair of DSBs by HR. 相似文献
98.
99.
Julie M. Bianchini Khameeka N. Kitt Martijn Gloerich Sabine Pokutta William I. Weis W. James Nelson 《The Journal of cell biology》2015,210(7):1065-1074
As part of the E-cadherin–β-catenin–αE-catenin complex (CCC), mammalian αE-catenin binds F-actin weakly in the absence of force, whereas cytosolic αE-catenin forms a homodimer that interacts more strongly with F-actin. It has been concluded that cytosolic αE-catenin homodimer is not important for intercellular adhesion because E-cadherin/αE-catenin chimeras thought to mimic the CCC are sufficient to induce cell–cell adhesion. We show that, unlike αE-catenin in the CCC, these chimeras homodimerize, bind F-actin strongly, and inhibit the Arp2/3 complex, all of which are properties of the αE-catenin homodimer. To more accurately mimic the junctional CCC, we designed a constitutively monomeric chimera, and show that E-cadherin–dependent cell adhesion is weaker in cells expressing this chimera compared with cells in which αE-catenin homodimers are present. Our results demonstrate that E-cadherin/αE-catenin chimeras used previously do not mimic αE-catenin in the native CCC, and imply that both CCC-bound monomer and cytosolic homodimer αE-catenin are required for strong cell–cell adhesion. 相似文献
100.
Callum R. Lawson Yngvild Vindenes Liam Bailey Martijn van de Pol 《Ecology letters》2015,18(7):724-736
Species' responses to environmental changes such as global warming are affected not only by trends in mean conditions, but also by natural and human‐induced environmental fluctuations. Methods are needed to predict how such environmental variation affects ecological and evolutionary processes, in order to design effective strategies to conserve biodiversity under global change. Here, we review recent theoretical and empirical studies to assess: (1) how populations respond to changes in environmental variance, and (2) how environmental variance affects population responses to changes in mean conditions. Contrary to frequent claims, empirical studies show that increases in environmental variance can increase as well as decrease long‐term population growth rates. Moreover, environmental variance can alter and even reverse the effects of changes in the mean environment, such that even if environmental variance remains constant, omitting it from population models compromises their ability to predict species' responses to changes in mean conditions. Drawing on theory relating these effects of environmental variance to the curvatures of population growth responses to the environment, we outline how species' traits such as phylogenetic history and body mass could be used to predict their responses to global change under future environmental variability. 相似文献