A casein kinase 1 prevents expulsion of the oocyte meiotic spindle into a polar body by regulating cortical contractility.

During female meiosis, haploid eggs are generated from diploid oocytes. This reduction in chromosome number occurs through two highly asymmetric cell divisions, resulting in one large egg and two small polar bodies. Unlike mitosis, where an actomyosin contractile ring forms between the sets of segregating chromosomes, the meiotic contractile ring forms on the cortex adjacent to one spindle pole, then ingresses down the length of the spindle to position itself at the exact midpoint between the two sets of segregating chromosomes. Depletion of casein kinase 1 gamma (CSNK-1) in Caenorhabditis elegans led to the formation of large polar bodies that contain all maternal DNA, because the contractile ring ingressed past the spindle midpoint. Depletion of CSNK-1 also resulted in the formation of deep membrane invaginations during meiosis, suggesting an effect on cortical myosin. Both myosin and anillin assemble into dynamic rho-dependent cortical patches that rapidly disassemble in wild-type embryos. CSNK-1 was required for disassembly of both myosin patches and anillin patches. Disassembly of anillin patches was myosin independent, suggesting that CSNK-1 prevents expulsion of the entire meiotic spindle into a polar body by negatively regulating the rho pathway rather than through direct inhibition of myosin

Membrane invaginations reveal cortical sites that pull on mitotic spindles in one-cell C. elegans embryos.

Asymmetric positioning of the mitotic spindle in C. elegans embryos is mediated by force-generating complexes that are anchored at the plasma membrane and that pull on microtubules growing out from the spindle poles. Although asymmetric distribution of the force generators is thought to underlie asymmetric positioning of the spindle, the number and location of the force generators has not been well defined. In particular, it has not been possible to visualize individual force generating events at the cortex. We discovered that perturbation of the acto-myosin cortex leads to the formation of long membrane invaginations that are pulled from the plasma membrane toward the spindle poles. Several lines of evidence show that the invaginations, which also occur in unperturbed embryos though at lower frequency, are pulled by the same force generators responsible for spindle positioning. Thus, the invaginations serve as a tool to localize the sites of force generation at the cortex and allow us to estimate a lower limit on the number of cortical force generators within the cell

Antisymmetrization of a Mean Field Calculation of the T-Matrix

The usual definition of the prior(post) interaction $V(V^\prime )$ between projectile and target (resp. ejectile and residual target) being contradictory with full antisymmetrization between nucleons, an explicit antisymmetrization projector ${\cal A}$ must be included in the definition of the transition operator, $T\equiv V^\prime{\cal A}+V^\prime{\cal A}GV.$ We derive the suitably antisymmetrized mean field equations leading to a non perturbative estimate of $T$. The theory is illustrated by a calculation of forward $\alpha$-$\alpha$ scattering, making use of self consistent symmetries.Comment: 30 pages, no figures, plain TeX, SPHT/93/14

Local dimensions in Moran constructions

We study the dimensional properties of Moran sets and Moran measures in doubling metric spaces. In particular, we consider local dimensions and $L^q$-dimensions. We generalize and extend several existing results in this area.Comment: 13 page

Efficiency of cloud condensation nuclei formation from ultrafine particles

Atmospheric cloud condensation nuclei (CCN) concentrations are a key uncertainty in the assessment of the effect of anthropogenic aerosol on clouds and climate. The ability of new ultrafine particles to grow to become CCN varies throughout the atmosphere and must be understood in order to understand CCN formation. We have developed the Probability of Ultrafine particle Growth (PUG) model to answer questions regarding which growth and sink mechanisms control this growth, how the growth varies between different parts of the atmosphere and how uncertainties with respect to the magnitude and size distribution of ultrafine emissions translates into uncertainty in CCN generation. The inputs to the PUG model are the concentrations of condensable gases, the size distribution of ambient aerosol, particle deposition timescales and physical properties of the particles and condensable gases. It was found in most cases that condensation is the dominant growth mechanism and coagulation with larger particles is the dominant sink mechanism for ultrafine particles. In this work we found that the probability of a new ultrafine particle generating a CCN varies from <0.1% to ~90% in different parts of the atmosphere, though in the boundary layer a large fraction of ultrafine particles have a probability between 1% and 40%. Some regions, such as the tropical free troposphere, are areas with high probabilities; however, variability within regions makes it difficult to predict which regions of the atmosphere are most efficient for generating CCN from ultrafine particles. For a given mass of primary ultrafine aerosol, an uncertainty of a factor of two in the modal diameter can lead to an uncertainty in the number of CCN generated as high as a factor for eight. It was found that no single moment of the primary aerosol size distribution, such as total mass or number, is a robust predictor of the number of CCN ultimately generated. Therefore, a complete description of the emissions size distribution is generally required for global aerosol microphysics models

Characterization of 1-ACBP B-ACBP and PBR in oesophageal cancer

Faculty of Science; School of molecular and Cell Biology; MSC DissertationBackground: Cancer of the oesophagus ranks as the ninth most common malignancy in the world, and recent evidence shows that its incidence is increasing. Apoptosis is a process of programmed cell death, which is as essential as cell growth, for the maintenance of homeostasis. When these processes lose integration, such as cancer, then uncontrolled cell growth occurs. There are at least five ACBP subgroups and the two being focused on in this study is B-ACBP (brain specific) and 1-ACBP (found in nearly all tissues). ACBPs act as intracellular carrier-proteins for medium to long chain acyl-coA, mediating fatty acid transport to the mitochondrion for ß-oxidation. ACBPs are also believed to be putative ligands of PBR (Peripheral Benzodiazepine Receptor), and bound to this receptor facilitates mitochondrial membrane permeabilization giving the notion that it favours apoptosis. Aim: To establish the expression patterns of 1-ACBP, B-ACBP, and PBR in oesophageal cancer, and to characterize their roles in this disease. Methodology: Paraffin-embedded sections of normal and malignant oesophageal tissues were utilized for localization studies. RNA probes was synthesized and labelled using Digoxigenin for colorimetric and fluorescent detection during the in situ hybridization (ISH) technique for localization. Real time quantitative RT-PCR was performed to determine the expression levels of the three genes in oesophageal cancer RNA using the Roche Lightcylcer .Results: All three genes showed substantial upregulation within the malignant tissue sections compared to normal oesophageal sections, all three transcripts localized specifically to plasma cells and lymphocytes in diseased and normal tissue section. In the diseased tissue B-ACBP and 1-ACBP mRNA localized to endothelial cells of blood vessels in the submucosa. B-ACBP also localized to the nucleus of squamous epithelium cells. PBR localization occurred in tumour islands in invasive tissue sections. Quantitative RT-PCR also illustrated PBR expression level was the highest compared to the ACBP genes expression in tumours. Conclusion: These results show that 1-ACBP, B-ACBP and PBR play a role in the pathogenesis of oesophageal cancer as well as immunology. Further experiments are still required to determine the function of these genes and the role they play in apoptosis and oesophageal cancer

A weak turbulence theory for incompressible magnetohydrodynamics

We derive a weak turbulence formalism for incompressible magnetohydrodynamics. Three-wave interactions lead to a system of kinetic equations for the spectral densities of energy and helicity. The kinetic equations conserve energy in all wavevector planes normal to the applied magnetic field B0ê[parallel R: parallel]. Numerically and analytically, we find energy spectra E± [similar] kn±[bot bottom], such that n+ + n− = −4, where E± are the spectra of the Elsässer variables z± = v ± b in the two-dimensional case (k[parallel R: parallel] = 0). The constants of the spectra are computed exactly and found to depend on the amount of correlation between the velocity and the magnetic field. Comparison with several numerical simulations and models is also made