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Lipids in marine sediments have been widely used in proxies to reconstruct Sea Surface Temperatures (SSTs). For example, the U_37^K proxy, based on the degree of unsaturation of long chain alkenones synthesized by haptophytes, the TEX86, based on glycerol dialkyl glycerol tetraethers (GDGTs) produced by Thaumarchaeota and the LDI, based on long chain diols by Eustigmatophyte algae. However, there is still some uncertainty regarding the biological producers of these lipids and their biosynthetic pathways. In this thesis, the pelagic and benthic archaeal community composition was investigated in multiple marine regions and compared it with the composition of GDGTs. This showed that Marine Group II Euryarchaeota, one of the most abundant marine archaeal groups, are incapable of producing these lipids. Studying three water columns in the Mediterranean Sea indicated the presence of deep-water Thaumarchaeota, which are potentially responsible for the overestimation of reconstructed SSTs in this region. Further, the biosynthetic pathway of long chain alkenones was investigated in a culture of the Haptophyte Emiliania huxleyi and identified a potential gene coding for the desaturase responsible for transforming C37:2 into C37:3 alkenones. In the African Lake Challa, a correlation was observed between the abundance of LCDs and uncultured Eustigmatophyceae algae. Besides, seasonal changes in LCD composition suggest multiple producers or changes in the LCD composition of the same producer within an annual cycle. The combination of omic (lipid and DNA) approaches in this thesis has proven to be key in increasing our knowledge on the biological producers of lipids involved in paleotemperature proxies.

The article hasn't a creative commons license associated nor informations about funders/sponsors. There is no public supplementary material available. Cancer cells frequently induce aberrant centrosomes, which have been implicated in cancer initiation and progression. Human colorectal cancer cells, HCT116, contain aberrant centrioles composed of disorganized cylindrical microtubules and displaced appendages. These cells also express unique centrosome-related structures associated with a subset of centrosomal components, including gamma-tubulin, centrin and PCM1. During hydroxyurea treatment, these abnormal structures become more abundant and undergo a change in shape from small dots to elongated fibers. Although gamma-tubulin seems to exist as a ring complex, the abnormal structures do not support microtubule nucleation. Several lines of evidence suggest that the fibers correspond to a disorganized form of centriolar microtubules. Plk4, a mammalian homolog of ZYG-1 essential for initiation of centriole biogenesis, is not associated with the gamma-tubulin-specific abnormal centrosomes. The amount of Plk4 at each centrosome was less in cells with abnormal centrosomes than cells without gamma-tubulin-specific abnormal centrosomes. In addition, the formation of abnormal structures was abolished by expression of exogenous Plk4, but not SAS6 and Cep135/Bld10p, which are downstream regulators required for the organization of nine-triplet microtubules. These results suggest that HCT116 cells fail to organize the ninefold symmetry of centrioles due to insufficient Plk4. There are no funders and sponsors indicated explicitly in the document. info:eu-repo/semantics/publishedVersion

We present a new assay for analyzing the specific binding of proteins to lipid ligands contained within vesicles or micelles. This assay, referred to as the electrophoretic migration shift assay, was developed using a model system composed of cholera toxin and of its physiological receptor, monosialoganglioside G M1 Using polyacrylamide gel electrophoresis in non-denaturing conditions, the migration of toxin components known to interact with G M1 was retarded when G M1 was present in either lipid vesicles or micelles. This effect was specific, as the migration of proteins not interacting with G M1 was not modified. The localization of retarded proteins and of lipids on gels was further determined by autoradiography. The stoichiometry of binding between cholera toxin and G M1 was determined, giving a value of five G M1 per one pentameric assembly of cholera toxin B-subunits, in agreement with previous studies. The general applicability of this assay was further established using both streptavidin and annexin V together with specific lipid ligands. This assay is fast, simple, quantitative, and requires only microgram quantities of protein.

Primary microcephaly is a rare condition in which brain size is substantially diminished without other syndromic abnormalities. Seven autosomal loci have been genetically mapped, and the underlying causal genes have been identified for MCPH1, MCPH3, MCPH5, MCPH6, and MCPH7 but not for MCPH2 or MCPH4. The known genes play roles in mitosis and cell division. We ascertained three families from an Eastern Canadian subpopulation, each with one microcephalic child. Homozygosity analysis in two families using genome-wide dense SNP genotyping supported linkage to the published MCPH4 locus on chromosome 15q21.1. Sequencing of coding exons of candidate genes in the interval identified a nonconservative amino acid change in a highly conserved residue of the centrosomal protein CEP152. The affected children in these two families were both homozygous for this missense variant. The third affected child was compound heterozygous for the missense mutation plus a second, premature-termination mutation truncating a third of the protein and preventing its localization to centrosomes in transfected cells. CEP152 is the putative mammalian ortholog of Drosphila asterless, mutations in which affect mitosis in the fly. Published data from zebrafish are also consistent with a role of CEP152 in centrosome function. By RT-PCR, CEP152 is expressed in the embryonic mouse brain, similar to other MCPH genes. Like some other MCPH genes, CEP152 shows signatures of positive selection in the human lineage. CEP152 is a strong candidate for the causal gene underlying MCPH4 and may be an important gene in the evolution of human brain size.

This thesis examines the hypothesis that American strategic nuclear doctrine since 1965 has been significantly influenced by multiple domestic variables. This analysis begins with an examination of the changes in American strategic doctrine, as expressed in the Secretary of Defense' s annual statement, between 1965-1980. The relationships which precipitated these changes are explored in terms of the following domestic variables (1) American perceptions of the Soviet threat (2) Strategic weapons system development (3) American public opinion (4) The personalities of key American policymakers (5) The Vietnam War Because of the complex inter-relationship between these variables, the modification of strategic doctrine can be accomplished only incrementally and thus rapid doctrinal change is virtually beyond the control of "grand strategists." http://archive.org/details/domesticdetermin00helg Lieutenant Commander, United States Navy Approved for public release; distribution is unlimited.