64 research outputs found
Perspective from a Younger Generation -- The Astro-Spectroscopy of Gisbert Winnewisser
Gisbert Winnewisser's astronomical career was practically coextensive with
the whole development of molecular radio astronomy. Here I would like to pick
out a few of his many contributions, which I, personally, find particularly
interesting and put them in the context of newer results.Comment: 14 pages. (Co)authored by members of the MPIfR (Sub)millimeter
Astronomy Group. To appear in the Proceedings of the 4th
Cologne-Bonn-Zermatt-Symposium "The Dense Interstellar Medium in Galaxies"
eds. S. Pfalzner, C. Kramer, C. Straubmeier, & A. Heithausen (Springer:
Berlin
Kinetochore fiber formation in animal somatic cells : dueling mechanisms come to a draw
Author Posting. © The Author, 2005. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Chromosoma 114 (2005): 310-318, doi:10.1007/s00412-005-0028-2.The attachment to and movement of a chromosome on the mitotic spindle is
mediated by the formation of a bundle of microtubules (MTs) that tethers the
kinetochore on the chromosome to a spindle pole. The origin of these “kinetochore
fibers” (K-fibers) has been investigated for over 125 years. As noted in 1944 by
Schrader, there are only three possible ways to form a K-fiber: either it a) grows from
the pole until it contacts the kinetochore; b) grows directly from the kinetochore; or c)
it forms as a result of an interaction between the pole and the chromosome. Since
Schrader’s time it has been firmly established that K-fibers in centrosome-containing
animal somatic cells form as kinetochores capture MTs growing from the spindle pole
(route a). It is now similarly clear that in cells lacking centrosomes, including plants
and many animal oocytes, K-fibers “self-assemble” from MTs generated by the
chromosomes (route b). Can animal somatic cells form K-fibers in the absence of
centrosomes by the “self-assembly” pathway? In 2000 the answer to this question
was shown to be a resounding “yes”. With this result, the next question became
whether the presence of a centrosome normally suppresses K-fiber self-assembly, or
if this route works concurrently with centrosome-mediated K-fiber formation. This
question, too, has recently been answered: observations on untreated live animal cells
expressing GFP-tagged tubulin clearly show that kinetochores can nucleate the
formation of their associated MTs in the presence of functional centrosomes. The
concurrent operation of these two “dueling” routes for forming K-fibers in animals
helps explain why the attachment of kinetochores and the maturation of K-fibers
occur as quickly as it does on all chromosomes within a cell.The work is sponsored by
NIH grant GMS 40198
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
Mechanisms of Chemoprotection against Aflatoxin-Induced Hepatocarcinogenesis by Oltipraz
Mortality of the Bryozoan Pentapora fascialis in the Ligurian Sea (NW Mediterranean) after Disturbance
Numerical Analysis of Free-Edge Effect on Size-Influenced Mechanical Properties of Single-Layer Triaxially Braided Composites
Interrelation between the spatial disposition of actin filaments and microtubules during the differentiation of tracheary elements in culturedZinnia cells
Deterring delinquents with information. Evidence from a randomized poster campaign in Bogotá
Crude Oil Sensing using Carbon Nano Structures Synthetized from Phoenix Dactylifera L. Cellulose
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