Books

Oral cancer Oral Cancer: Epidemiology, Etiology and Pathology. Ed. by Colin Smith, Jens Pindborg and W. H. Binnie. Pp. ix + 106. Illustrated. R183,30. USA: Hemisphere. 1990.HPV and cervical cancer Human Papillomavirus and Cervical Cancer. Ed. by N. Munoz, F. X. Bosch and O. M. Jensen. Pp. xii + 155. Illustrated. France: International Agency for Research on Cancer. 1989.Child health Child Health in a Multicultural Society. Ed. by John Black. Pp. 75. Illustrated. £7 (including postage). London: BMJ. 1989. (Available also from Libriger Book Distributors).Merck manual of geriatics Merck Manual of Geriatrics. Ed. by William B. Abrams The Andrew J. Fletcher. Pp. xxii + 1267. Illustrated. RI4,50. and I: Merck. 1990. USALiver disease Progress in Liver Diseases. Vol 9. Ed. by Hans Popper and Fenton Schaffner. Pp. xv + 750. Illustrated. RllO. England: Harcourt Brace Jovanovich. 1990.Clinical dietetics and nutrition Clinical Dietetics and Nutrition. 3rd ed. Ed. by F. P. Antia. Pp. xvi +438. Illustrated. Oxford: Oxford University Press. 1989.Atlas of human anatomy Wolf-Heidegger's Atlas of Human Anatomy. Ed. by H. F. Frick, B. Kummer and R. V. Putz. pp. viii + 599. £(j(J. Basel: Karger. 1990.Health system decentralisation Health System Decentralization. Ed. by A. Mills, J. P. Vaughan, D. L. Smith and I. Tabibzadcll. pp. 151. Illustrated. SFr. 26. Geneva: World Health Organisation. 1990.Handbook of occupational medicine Handbook of Occupational Medicine. Ed. by Robert J. McCunney. Pp. xxiii + 510. Illustrated. Boston: Little, Brown. 1988.Leukaemia Leukaemia. 5th ed. Ed. by Edward S. Henderson and T. Andrew Lister. Pp. vii + 821. Illustrated. RHO. Kent: Harcoun Brace Jovanovich. 1990

Tertiary sequence of deformation in a thin-skinned/thick-skinned collision belt: The Zagros Folded Belt (Fars, Iran)

International audienceWe describe how thin-skinned/thick-skinned deformation in the Zagros Folded Belt interacted in time and space. Homogeneous fold wavelengths (15.8 ± 5.3 km), tectono-sedimentary evidence for simultaneous fold growth in the past 5.5 ± 2.5 Ma, drainage network organization, and homogeneous peak differential stresses (40 ± 15 MPa) together point to buckling as the dominant process responsible for cover folding. Basin analysis reveals that basement inversion occurred ∼20 Ma ago as the Arabia/Eurasian plate convergence reduced and accumulation of Neogene siliciclastics in foreland basin started. By 10 Ma, ongoing contraction occurred by underplating of Arabian crustal units beneath the Iranian plate. This process represents 75% of the total shortening. It is not before 5 Ma that the Zagros foreland was incorporated into the southward propagating basement thrust wedge. Folds rejuvenated by 3–2 Ma because of uplift driven by basement shortening and erosion. Since then, folds grew at 0.3—0.6 mm/yr and forced the rivers to flow axially. A total shortening of 65–78 km (16–19%) is estimated across the Zagros. This corresponds to shortening rates of 6.5–8 km/Ma consistent with current geodetic surveys. We point out that although thin-skinned deformation in the sedimentary cover may be important, basement-involved shortening should not be neglected as it requires far less shortening. Moreover, for such foreland folded belts involving basement shortening, underplating may be an efficient process accommodating a significant part of the plate convergence

Mouse TRIP13/PCH2 Is Required for Recombination and Normal Higher-Order Chromosome Structure during Meiosis

Accurate chromosome segregation during meiosis requires that homologous chromosomes pair and become physically connected so that they can orient properly on the meiosis I spindle. These connections are formed by homologous recombination closely integrated with the development of meiosis-specific, higher-order chromosome structures. The yeast Pch2 protein has emerged as an important factor with roles in both recombination and chromosome structure formation, but recent analysis suggested that TRIP13, the mouse Pch2 ortholog, is not required for the same processes. Using distinct Trip13 alleles with moderate and severe impairment of TRIP13 function, we report here that TRIP13 is required for proper synaptonemal complex formation, such that autosomal bivalents in Trip13-deficient meiocytes frequently displayed pericentric synaptic forks and other defects. In males, TRIP13 is required for efficient synapsis of the sex chromosomes and for sex body formation. Furthermore, the numbers of crossovers and chiasmata are reduced in the absence of TRIP13, and their distribution along the chromosomes is altered, suggesting a role for TRIP13 in aspects of crossover formation and/or control. Recombination defects are evident very early in meiotic prophase, soon after DSB formation. These findings provide evidence for evolutionarily conserved functions for TRIP13/Pch2 in both recombination and formation of higher order chromosome structures, and they support the hypothesis that TRIP13/Pch2 participates in coordinating these key aspects of meiotic chromosome behavior

The SMC-5/6 Complex and the HIM-6 (BLM) Helicase Synergistically Promote Meiotic Recombination Intermediate Processing and Chromosome Maturation during<i> Caenorhabditis elegans</i> Meiosis

Meiotic recombination is essential for the repair of programmed double strand breaks (DSBs) to generate crossovers (COs) during meiosis. The efficient processing of meiotic recombination intermediates not only needs various resolvases but also requires proper meiotic chromosome structure. The Smc5/6 complex belongs to the structural maintenance of chromosome (SMC) family and is closely related to cohesin and condensin. Although the Smc5/6 complex has been implicated in the processing of recombination intermediates during meiosis, it is not known how Smc5/6 controls meiotic DSB repair. Here, using Caenorhabditis elegans we show that the SMC-5/6 complex acts synergistically with HIM-6, an ortholog of the human Bloom syndrome helicase (BLM) during meiotic recombination. The concerted action of the SMC-5/6 complex and HIM-6 is important for processing recombination intermediates, CO regulation and bivalent maturation. Careful examination of meiotic chromosomal morphology reveals an accumulation of inter-chromosomal bridges in smc-5; him-6 double mutants, leading to compromised chromosome segregation during meiotic cell divisions. Interestingly, we found that the lethality of smc-5; him-6 can be rescued by loss of the conserved BRCA1 ortholog BRC-1. Furthermore, the combined deletion of smc-5 and him-6 leads to an irregular distribution of condensin and to chromosome decondensation defects reminiscent of condensin depletion. Lethality conferred by condensin depletion can also be rescued by BRC-1 depletion. Our results suggest that SMC-5/6 and HIM-6 can synergistically regulate recombination intermediate metabolism and suppress ectopic recombination by controlling chromosome architecture during meiosis

Genome-Wide Crossover Distribution in Arabidopsis thaliana Meiosis Reveals Sex-Specific Patterns along Chromosomes

In most species, crossovers (COs) are essential for the accurate segregation of homologous chromosomes at the first meiotic division. Their number and location are tightly regulated. Here, we report a detailed, genome-wide characterization of the rate and localization of COs in Arabidopsis thaliana, in male and female meiosis. We observed dramatic differences between male and female meiosis which included: (i) genetic map length; 575 cM versus 332 cM respectively; (ii) CO distribution patterns: male CO rates were very high at both ends of each chromosome, whereas female CO rates were very low; (iii) correlations between CO rates and various chromosome features: female CO rates correlated strongly and negatively with GC content and gene density but positively with transposable elements (TEs) density, whereas male CO rates correlated positively with the CpG ratio. However, except for CpG, the correlations could be explained by the unequal repartition of these sequences along the Arabidopsis chromosome. For both male and female meiosis, the number of COs per chromosome correlates with chromosome size expressed either in base pairs or as synaptonemal complex length. Finally, we show that interference modulates the CO distribution both in male and female meiosis

Free-standing polyelectrolyte membranes made of chitosan and alginate

Free-standing films have increasing applications in the biomedical field as drug delivery systems for wound healing and tissue engineering. Here, we prepared free-standing membranes by the layer-by-layer assembly of chitosan and alginate, two widely used biomaterials. Our aim was to produce a thick membrane and to study the permeation of model drugs and the adhesion of muscle cells. We first defined the optimal growth conditions in terms of pH and alginate concentration. The membranes could be easily detached from polystyrene or polypropylene substrate without any postprocessing step. The dry thickness was varied over a large range from 4 to 35 μm. A 2-fold swelling was observed by confocal microscopy when they were immersed in PBS. In addition, we quantified the permeation of model drugs (fluorescent dextrans) through the free-standing membrane, which depended on the dextran molecular weight. Finally, we showed that myoblast cells exhibited a preferential adhesion on the alginate-ending membrane as compared to the chitosan-ending membrane or to the substrate side.This work was financially supported by Foundation for Science and Technology (FCT) through the Scholarship SFRH/BD/64601/2009 granted to S.G.C. C.M. is indebted to Grenoble INP for financial support via a postdoctoral fellowship. This work was supported by the European Commission (FP7 Program) via a European Research Council starting grant (BIOMIM, GA 259370 to C.P.). C.P. is also grateful to Institut Universitaire de France and to Grenoble Institute of Technology for financial support. We thank Isabelle Paintrand for her technical help with the confocal apparatus and Patrick Chaudouet for his help with SEM imaging