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101.
Aflatoxin contamination of maize by Aspergillus flavus poses serious potential economic losses in the US and health hazards to humans, particularly in West Africa. The Southern
Regional Research Center of the United States Department of Agriculture, Agricultural Research Service (USDA-ARS-SRRC) and
the International Institute of Tropical Agriculture (IITA) initiated a collaborative breeding project to develop maize germplasm
with resistance to aflatoxin accumulation. Resistant genotypes from the US and selected inbred lines from IITA were used to
generate backcrosses with 75% US germplasm and F1 crosses with 50% IITA and 50% US germplasm. A total of 65 S4 lines were developed from the backcross populations and 144 S4 lines were derived from the F1 crosses. These lines were separated into groups and screened in SRRC laboratory using a kernel-screening assay. Significant
differences in aflatoxin production were detected among the lines within each group. Several promising S4 lines with aflatoxin values significantly lower than their respective US resistant recurrent parent or their elite tropical
inbred parent were selected for resistance-confirmation tests. We found pairs of S4 lines with 75–94% common genetic backgrounds differing significantly in aflatoxin accumulation. These pairs of lines are
currently being used for proteome analysis to identify resistance-associated proteins and the corresponding genes underlying
resistance to aflatoxin accumulation. Following confirmation tests in the laboratory, lines with consistently low aflatoxin
levels will be inoculated with A. flavus in the field in Nigeria to identify lines resistant to strains specific to both US and West Africa. Maize inbred lines with
desirable agronomic traits and low levels of aflatoxin in the field would be released as sources of genes for resistance to
aflatoxin production. 相似文献
102.
J. Yu T. E. Cleveland J. R. Wilkinson B. C. Campbell J. H. Kim H. S. Kim D. Bhatnagar G. A. Payne W. C. Nierman 《Mycotoxin Research》2006,22(1):16-21
Aflatoxins are the most toxic and carcinogenic naturally occurring mycotoxins. They are produced primarily byAspergillus flavus andA. parasiticus. In order to better understand the molecular mechanisms that control aflatoxin production, identification of genes usingA. flavus expressed sequence tags (ESTs) and microarrays is currently being performed. Sequencing and annotation ofA. flavus ESTs from a normalizedA. flavus cDNA library identified 7,218 unique EST sequences. Genes that are putatively involved in aflatoxin biosynthesis, regulation
and signal transduction, fungal virulence or pathogenicity, stress response or antioxidation, and fungal development were
identified from these ESTs. Microarrays containing over 5,000 uniqueA. flavus gene amplicons were constructed at The Institute for Genomic Research. Gene expression profiling under aflatoxin-producing
and non-producing conditions using this microarray has identified hundreds of genes that are potentially involved in aflatoxin
production. Further investigations on the functions of these genes by gene knockout experiments are underway. This research
is expected to provide information for developing new strategies for controlling aflatoxin contamination of agricultural commodities. 相似文献
103.
104.
Andrew J. Holland Weijie Lan Sherry Niessen Heather Hoover Don W. Cleveland 《The Journal of cell biology》2010,188(2):191-198
Accurate control of the number of centrosomes, the major microtubule-organizing centers of animal cells, is critical for the maintenance of genome integrity. Abnormalities in centrosome number can promote errors in spindle formation that lead to subsequent chromosome missegregation, and extra centrosomes are found in many cancers. Centrosomes are comprised of a pair of centrioles surrounded by amorphous pericentriolar material, and centrosome duplication is controlled by centriole replication. Polo-like kinase 4 (Plk4) plays a key role in initiating centriole duplication, and overexpression of Plk4 promotes centriole overduplication and the formation of extra centrosomes. Using chemical genetics, we show that kinase-active Plk4 is inherently unstable and targeted for degradation. Plk4 is shown to multiply self-phosphorylate within a 24–amino acid phosphodegron. Phosphorylation of multiple sites is required for Plk4 instability, indicating a requirement for a threshold level of Plk4 kinase activity to promote its own destruction. We propose that kinase-mediated, autoregulated instability of Plk4 self-limits Plk4 activity so as to prevent centrosome amplification. 相似文献
105.
Insertion and truncation of c-myb by murine leukemia virus in a myeloid cell line derived from cultures of normal hematopoietic cells. 总被引:13,自引:4,他引:9 下载免费PDF全文
A retroviral insertion into the c-myb gene, which resulted in a 3' truncation, was found in an in vitro-derived myeloid cell line. The retroviral insertion occurred at precisely the same nucleotide at which another murine leukemia virus insertion occurred in an in vivo-induced myeloid leukemia. These findings suggest that comparable events may be required for the derivation of myeloid cell lines in vitro and for induction of myeloid leukemia in vivo. 相似文献
106.
107.
Essential role of phospholipase C gamma 2 in early B-cell development and Myc-mediated lymphomagenesis 下载免费PDF全文
Wen R Chen Y Bai L Fu G Schuman J Dai X Zeng H Yang C Stephan RP Cleveland JL Wang D 《Molecular and cellular biology》2006,26(24):9364-9376
Phospholipase Cgamma2 (PLCgamma2) is a critical signaling effector of the B-cell receptor (BCR). Here we show that PLCgamma2 deficiency impedes early B-cell development, resulting in an increase of B220+ CD43+ BP-1+ CD24hi pre-BCR+ large pre-B cells. PLCgamma2 deficiency impairs pre-BCR-mediated functions, leading to enhanced interleukin-7 (IL-7) signaling and elevated levels of RAGs in the selected large pre-B cells. Consequently, PLCgamma2 deficiency renders large pre-B cells susceptible to transformation, resulting in dramatic acceleration of Myc-induced lymphomagenesis. PLCgamma2(-/-) Emu-Myc transgenic mice mainly develop lymphomas of B220+ CD43+ BP-1+ CD24hi pre-BCR+ large pre-B-cell origin, which are uncommon in wild-type Emu-Myc transgenics. Furthermore, lymphomas from PLCgamma2(-/-) Emu-Myc transgenic mice exhibited a loss of p27Kip1 and often displayed alterations in Arf or p53. Thus, PLCgamma2 plays an important role in pre-BCR-mediated early B-cell development, and its deficiency leads to markedly increased pools of the most at-risk large pre-B cells, which display hyperresponsiveness to IL-7 and express high levels of RAGs, making them prone to secondary mutations and Myc-induced malignancy. 相似文献
108.
109.
Sarah R. Sattin Cory C. Cleveland Eran Hood Sasha C. Reed Andrew J. King Steven K. Schmidt Michael S. Robeson Nataly Ascarrunz Diana R. Nemergut 《Journal of microbiology (Seoul, Korea)》2009,47(6):673-681
Past work in recently deglaciated soils demonstrates that microbial communities undergo shifts prior to plant colonization.
To date, most studies have focused on relatively ‘long’ chronosequences with the ability to sample plant-free sites over at
least 50 years of development. However, some recently deglaciated soils feature rapid plant colonization and questions remain
about the relative rate of change in the microbial community in the unvegetated soils of these chronosequences. Thus, we investigated
the forelands of the Mendenhall Glacier near Juneau, AK, USA, where plants rapidly establish. We collected unvegetated samples
representing soils that had been ice-free for 0, 1, 4, and 8 years. Total nitrogen (N) ranged from 0.00∼0.14 mg/g soil, soil
organic carbon pools ranged from 0.6∼2.3 mg/g soil, and both decreased in concentration between the 0 and 4 yr soils. Biologically
available phosphorus (P) and pH underwent similar dynamics. However, both pH and available P increased in the 8 yr soils.
Nitrogen fixation was nearly undetectable in the most recently exposed soils, and increased in the 8 yr soils to ∼5 ng N fixed/cm2/h, a trend that was matched by the activity of the soil N-cycling enzymes urease and β-l,4-N-acetyl-glucosa-minidase. 16S
rRNA gene clone libraries revealed no significant differences between the 0 and 8 yr soils; however, 8 yr soils featured the
presence of cyanobacteria, a division wholly absent from the 0 yr soils. Taken together, our results suggest that microbes
are consuming allochtonous organic matter sources in the most recently exposed soils. Once this carbon source is depleted,
a competitive advantage may be ceded to microbes not reliant on in situ nutrient sources. 相似文献
110.
In interphase and mitosis, centrosomes play a major role in the spatial organization of the microtubule network. Alterations in centrosome number and structure are associated with genomic instability and occur in many cancers. Centrosome duplication is controlled by centriole replication. In most dividing animal cells, centrioles duplicate only once per cell cycle at a site adjacent to existing centrioles. The conserved protein kinase Polo-like kinase 4 (Plk4) has a key role in controlling centriole biogenesis. Overexpression of Plk4 drives centrosome amplification and is associated with tumorigenesis in flies. By contrast, haploinsufficiency of Plk4 promotes cytokinesis failure, leading to an increased incidence of tumors in mice. Recent studies have shown that Plk4 is a low abundance protein whose stability is linked to the activity of the enzyme. We discuss how this autoregulatory feedback loop acts to limit the damaging effects caused by too much or too little Plk4.Key words: centrosome, centriole, polo-like kinase 4, Plk4, SAK, SCF, phosphodegron, β-TrCP, aneuploidyCentrosomes are the major microtubule organizing centers of animal cells and play a particularly important role during mitosis where they organize the two opposite poles of the bipolar microtubule spindle apparatus upon which chromosomes are segregated. Although centrosomes are not strictly essential for the formation of the mitotic/meiotic spindle, whenever they are present they play a dominant role in guiding spindle formation.1,2 Extra copies of centrosomes frequently result in errors in spindle assembly that give rise to chromosome missegregation and the production of aneuploid daughter cells.3,4 Almost one hundred years ago, Theodor Boveri proposed that centrosome amplification can contribute to tumorigenesis.5 Since then supernumerary centrosomes have been reported in a variety of different tumor cells in vitro and in vivo and are a consistent feature of aneuploid tumors.6–13 However, despite the large body of circumstantial evidence linking extra centrosomes to the development of cancer, it remains unclear whether supernumerary centrosomes actively contribute to tumorigenesis or arise as a byproduct of cellular transformation. 相似文献