Stubble Losses of Kentucky Soybeans

Double crop soybeans in Kentucky tend to be shorter than plants from full season plantings. Since lowest pod height is related to plant height, double crop soybeans may be subject to greater harvest losses due to pods remaining below the level at which the combine header is operated. While it would be possible to lower the header closer to the soil to pick up some of those pods, that would slow down harvest and increase the risk of picking up stones and other trash. Although the actual cutting heights used in Kentucky are not known, some producers use combines with flexible ground-hugging headers, and others use nonflexible headers. Regardless of header type, some producers cut higher to avoid stones or to complete harvest more quickly

Does Chemical Leaf Burn of Double Crop Soybeans Reduce Yield?

Most farmers who have applied acifluorfen (sold as Blazer or Tackle) for postemergence control of broadleaf weeds in soybean fields are aware that leaf crinkling, bronzing, and necrosis can result. Despite this, studies in Kentucky, Illinois, Arkansas, and South Carolina have shown that full season soybeans have plenty of time to recover from leaf burn caused by this herbicide, and no yield losses have been found. However, double crop soybeans are usually planted much later than the full season crop. This delay in planting may reduce the time for plants to complete vegetative growth before beginning the seed production process. Therefore, double crop soybeans may be limited in their ability to recover from acifluorfen injury in time to produce as much grain as nonsprayed soybeans. Our objective was to determine if yields of double crop soybeans are reduced by leaf burn due to the use of acifluorfen

The fate of the homoctenids (Tentaculitoidea) during the Frasnian-Famennian mass extinction (Late Devonian)

The homoctenids (Tentaculitoidea) are small, conical-shelled marine animals which are amongst the most abundant and widespread of all Late Devonian fossils. They were a principal casualty of the Frasnian-Famennian (F-F, Late Devonian) mass extinction, and thus provide an insight into the extinction dynamics. Despite their abundance during the Late Devonian, they have been largely neglected by extinction studies. A number of Frasnian-Famennian boundary sections have been studied, in Poland, Germany, France, and the United States. These sections have yielded homoctenids, which allow precise recognition of the timing of the mass extinction. It is clear that the homoctenids almost disappear from the fossil record during the latest Frasnian “Upper Kellwasser Event”. The coincident extinction of this pelagic group, and the widespread development of intense marine anoxia within the water column, provides a causal link between anoxia and the F-F extinction. Most notable is the sudden demise of a group, which had been present in rock-forming densities, during this anoxic event. One new species, belonging to Homoctenus is described, but is not formally named here

The role of coxI -associated repeated sequences in plant mitochondrial DNA rearrangements and radish cytoplasmic male sterility

The gene coxI , encoding subunit I of mitochondrial cytochrome c oxidase, has been characterized from the normal (fertile) and Ogura (male-sterile) cytoplasms of radish to determine if a previously identified mitochondrial DNA rearrangement, and its associated transcriptional differences, could play a role in Ogura cytoplasmic male sterility (CMS). The normal and Ogura loci are virtually identical for 2.8 kb, including a 527-codon open reading frame whose product is approximately 95% identical to other plant COXI polypeptides. A rearrangement 120 bp 5′ to the coding region results in different 5′ transcript termini for the two genes. A comparison of several crucifer mitochondrial DNAs indicates that this rearrangement also occurs in the normal radish cytoplasm and is, therefore, not involved in Ogura CMS. Sequences present at the coxI locus belong to at least two different dispersed repeat families, members of which are also associated with other rearranged genes in radish.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46974/1/294_2004_Article_BF00336485.pd

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Processed pseudogenes acquired somatically during cancer development

Cancer evolves by mutation, with somatic reactivation of retrotransposons being one such mutational process. Germline retrotransposition can cause processed pseudogenes, but whether this occurs somatically has not been evaluated. Here we screen sequencing data from 660 cancer samples for somatically acquired pseudogenes. We find 42 events in 17 samples, especially non-small cell lung cancer (5/27) and colorectal cancer (2/11). Genomic features mirror those of germline LINE element retrotranspositions, with frequent target-site duplications (67%), consensus TTTTAA sites at insertion points, inverted rearrangements (21%), 5′ truncation (74%) and polyA tails (88%). Transcriptional consequences include expression of pseudogenes from UTRs or introns of target genes. In addition, a somatic pseudogene that integrated into the promoter and first exon of the tumour suppressor gene, MGA, abrogated expression from that allele. Thus, formation of processed pseudogenes represents a new class of mutation occurring during cancer development, with potentially diverse functional consequences depending on genomic context

Sentinel node micrometastases in breast cancer do not affect prognosis: a population-based study

International audienceSentinel node biopsy (SNB) for axillary staging in breast cancer allows the application of more extensive pathologic examination techniques. Micrometastases are being detected more often, however, coinciding with stage migration. Besides assessing the prognostic relevance of micrometastases and the need for administering adjuvant systemic and regional therapies, there still seems to be room for improvement. In a population-based analysis, we compared survival of patients with sentinel node micrometastases with those with node-negative and node-positive disease in the era after introduction of SNB. Data from the population-based Eindhoven Cancer Registry were used on all ( = 6803) women who underwent SNB for invasive breast cancer in the Southeast Region of The Netherlands in the period 1996-2006. In 451 patients (6.6%) a sentinel node micrometastasis (pN1mi) was detected and in 126 patients (1.9%) isolated tumor cells (pN0(i+)). Micrometastases or isolated tumor cells in the SNB did not convey any significant survival difference compared with node-negative disease. After adjustment for age, pT, and grade, still no survival difference emerged pN1mi: [HR 0.9 (95% CI, 0.6-1.3)] and pN0(i+): [HR 0.4 (95% CI, 0.14-1.3)] and neither was the case after additional adjustment for adjuvant systemic therapy. Our practice-based study showed that the presence of sentinel node micrometastases in breast cancer patients has hardly any impact on breast cancer overall survival during the first years after diagnosis

Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing

Chromothripsis is a mutational phenomenon characterized by massive, clustered genomic rearrangements that occurs in cancer and other diseases. Recent studies in selected cancer types have suggested that chromothripsis may be more common than initially inferred from low-resolution copy-number data. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), we analyze patterns of chromothripsis across 2,658 tumors from 38 cancer types using whole-genome sequencing data. We find that chromothripsis events are pervasive across cancers, with a frequency of more than 50% in several cancer types. Whereas canonical chromothripsis profiles display oscillations between two copy-number states, a considerable fraction of events involve multiple chromosomes and additional structural alterations. In addition to non-homologous end joining, we detect signatures of replication-associated processes and templated insertions. Chromothripsis contributes to oncogene amplification and to inactivation of genes such as mismatch-repair-related genes. These findings show that chromothripsis is a major process that drives genome evolution in human cancer