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101.
102.
Potential causes of arrested succession in Kibale National Park, Uganda: growth and mortality of seedlings 总被引:2,自引:0,他引:2
Colin A. Chapman Lauren J. Chapman Les Kaufman Amy E. Zanne 《African Journal of Ecology》1999,37(1):81-92
Recent studies suggest that regeneration following large-scale disturbance in Kibale National Park, Uganda, is slow or possibly arrested. Here, data is provided on the growth and mortality of seedlings in the forest understory, treefall gaps, and in large gaps that suggest that this pattern of arrested succession can be attributed partially to the fact that this East African community lacks aggressive colonizing tree species. Growth and mortality rates were contrasted for seedlings of six tree species planted in the understory, small gaps, and large gaps for 36 months. Data suggest that species are adapted to gaps of particular sizes. For example, Uvariopsis congensis grew faster in the understory than in small gaps, whereas Warburgia ugandensis had the lowest mortality rate and highest growth rate in large gaps. Seedlings (n=170) of 15 species were transplanted to assess the response of the tree community to large gap conditions. The limited survival of seedlings in large gaps relative to the understory suggests that only a small proportion of the tree community in this forest regenerates best in gaps larger than those created by the collapse of a single tree. These findings differ from a number of studies conducted in other geographical regions, and suggests that tree communities differ with respect to the proportion of tree species adapted to gaps of particular sizes. This may relate to variation among regions in their history of disturbance and thus frequency of gap formation, size of gaps, and the duration of periods of release. Such variation could imply the existence of a corresponding pattern among tropical forests of differential vulnerability to human disturbance, which tends to create many large gaps. 相似文献
103.
Pacheco-Oliver M McDonald IR Groleau D Murrell JC Miguez CB 《FEMS microbiology letters》2002,209(2):313-319
Tundra soil samples from the Canadian Arctic community, Kuujjuaq, were analyzed for the presence of the soluble (sMMO) and particulate (pMMO) methane monooxygenase genes. Total genomic DNA extracted from these soils was used as template for PCR using sMMO- and pMMO-specific primers, mmoX1-mmoX2 and A189-A682, respectively. pMMO and sMMO genes were detected in the Kuujjuaq soil samples. Isolation of sMMO-possessing methanotrophic microorganisms from the three soils, as determined by the colony naphthalene oxidation assay, was carried out using direct plating (5 degrees C) and methane enrichment studies (5 degrees C and 25 degrees C). Direct plating did not yield sMMO-possessing methanotrophic bacteria, whereas methane enrichments yielded isolates possessing and expressing sMMO activity. Analysis of derived amino acid sequences of pmoA genes and partial 16S rRNA genes obtained by PCR, using DNA isolated directly from this environment and from isolates, revealed the presence of highly divergent PmoA/AmoA sequences and 16S rRNA sequences that cluster closely with but are distinct from the genes from the genera Methylosinus and Methylocystis. 相似文献
104.
Holzapfel E Eisner G Alami M Barrett CM Buchanan G Lüke I Betton JM Robinson C Palmer T Moser M Müller M 《Biochemistry》2007,46(10):2892-2898
Translocation of twin-arginine precursor proteins across the cytoplasmic membrane of Escherichia coli requires the three membrane proteins TatA, TatB, and TatC. TatC and TatB were shown to be involved in precursor binding. We have analyzed in vitro a number of single alanine substitutions in tatC that were previously shown to compromise in vivo the function of the Tat translocase. All tatC mutants that were defective in precursor translocation into cytoplasmic membrane vesicles concomitantly interfered with precursor binding not only to TatC but also to TatB. Hence structural changes of TatC that affect precursor targeting simultaneously abolish engagement of the twin-arginine signal sequence with TatB and block the formation of a functional Tat translocase. Since these phenotypes were observed for tatC mutations spread over the first half of TatC, this entire part of the molecule must globally be involved in precursor binding. 相似文献
105.
Lipid droplets (LDs) were once viewed as simple, inert lipid micelles. However, they are now known to be organelles with a rich proteome involved in a myriad of cellular processes. LDs are heterogeneous in nature with different sizes and compositions of phospholipids, neutral lipids and proteins. This review takes a focused look at the roles of proteins involved in the regulation of LD formation, expansion, and morphology. The related proteins are summarized such as the fat-specific protein (Fsp27), fat storage-inducing trans- membrane (FIT) proteins, seipin and ADP-ribosylation factor 1-coat protein complex I (Arf-COPI). Finally, we present important challenges in LD biology for a deeper understanding of this dynamic organelle to be achieved. 相似文献
106.
Aldo Spanjaard Ronak Shah Daniël de
Groot Olimpia Alessandra Buoninfante Ben Morris Cor Lieftink Colin Pritchard Lisa
M Zürcher Shirley Ormel Joyce J I Catsman Renske de
Korte-Grimmerink Bjrn Siteur Natalie Proost Terry Boadum Marieke van
de
Ven Ji-Ying Song Maaike Kreft Paul C M van
den
Berk Roderick
L Beijersbergen Heinz Jacobs 《Nucleic acids research》2022,50(13):7420
Crosslink repair depends on the Fanconi anemia pathway and translesion synthesis polymerases that replicate over unhooked crosslinks. Translesion synthesis is regulated via ubiquitination of PCNA, and independently via translesion synthesis polymerase REV1. The division of labor between PCNA-ubiquitination and REV1 in interstrand crosslink repair is unclear. Inhibition of either of these pathways has been proposed as a strategy to increase cytotoxicity of platinating agents in cancer treatment. Here, we defined the importance of PCNA-ubiquitination and REV1 for DNA in mammalian ICL repair. In mice, loss of PCNA-ubiquitination, but not REV1, resulted in germ cell defects and hypersensitivity to cisplatin. Loss of PCNA-ubiquitination, but not REV1 sensitized mammalian cancer cell lines to cisplatin. We identify polymerase Kappa as essential in tolerating DNA damage-induced lesions, in particular cisplatin lesions. Polk-deficient tumors were controlled by cisplatin treatment and it significantly delayed tumor outgrowth and increased overall survival of tumor bearing mice. Our results indicate that PCNA-ubiquitination and REV1 play distinct roles in DNA damage tolerance. Moreover, our results highlight POLK as a critical TLS polymerase in tolerating multiple genotoxic lesions, including cisplatin lesions. The relative frequent loss of Polk in cancers indicates an exploitable vulnerability for precision cancer medicine. 相似文献
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