Prediction of channel connectivity and fluvial style in the flood basin successions of the Upper Permian Rangal Coal Measures (Queensland)

Predicting the presence and connectivity of reservoir-quality facies in otherwise mud-prone fluvial overbank successions is important because such sand bodies can potentially provide connectivity between larger neighboring sand bodies. This article addresses minor channelized fluvial elements (crevasse-splay and distributary channels) and attempts to predict the connectivity between such sand bodies in two interseam packages of the Upper Permian Rangal Coal Measures of northeastern Australia. Channel-body percent as measured in well logs was 2% in the upper (Aries-Castor) interseam and 17% in the lower (Castor-Pollux) interseam. Well spacing were too great to allow accurate correlation of channel bodies. The Ob River, Siberia, was used as a modern analog to supply planform geometric measurements of splay and distributary channels so that stochastic modeling of channel bodies was possible. The resulting models demonstrated that (1) channel-body connectivity is more uniform between minor distributary channels than between crevasse-splay channels; (2) relatively good connectivity is seen in proximal positions in splays but decreases distally from the source as channel elements diverge; and (3) connectivity tends to be greater down the axis of splays, with more isolated channel bodies occurring at the margins

Rad51 Paralogs Remodel Pre-synaptic Rad51 Filaments to Stimulate Homologous Recombination

SummaryRepair of DNA double strand breaks by homologous recombination (HR) is initiated by Rad51 filament nucleation on single-stranded DNA (ssDNA), which catalyzes strand exchange with homologous duplex DNA. BRCA2 and the Rad51 paralogs are tumor suppressors and critical mediators of Rad51. To gain insight into Rad51 paralog function, we investigated a heterodimeric Rad51 paralog complex, RFS-1/RIP-1, and uncovered the molecular basis by which Rad51 paralogs promote HR. Unlike BRCA2, which nucleates RAD-51-ssDNA filaments, RFS-1/RIP-1 binds and remodels pre-synaptic filaments to a stabilized, “open,” and flexible conformation, in which the ssDNA is more accessible to nuclease digestion and RAD-51 dissociation rate is reduced. Walker box mutations in RFS-1, which abolish filament remodeling, fail to stimulate RAD-51 strand exchange activity, demonstrating that remodeling is essential for RFS-1/RIP-1 function. We propose that Rad51 paralogs stimulate HR by remodeling the Rad51 filament, priming it for strand exchange with the template duplex

Sub‐annual moraine formation at an active temperate Icelandic glacier

This paper presents detailed geomorphological and sedimentological investigations of small recessional moraines at Fjallsjökull, an active temperate outlet of Öræfajökull, southeast Iceland. The moraines are characterised by striking sawtooth or hairpin planforms, which are locally superimposed, giving rise to a complex spatial pattern. We recognise two distinct populations of moraines, namely a group of relatively prominent moraine ridges (mean height ~1.2 m) and a group of comparatively low‐relief moraines (mean height ~0.4 m). These two groups often occur in sets/systems, comprising one pronounced outer ridge and several inset smaller moraines. Using a representative subsample of the moraines, we establish that they form by either (i) submarginal deformation and squeezing of subglacial till or (ii) pushing of extruded tills. Locally, proglacial (glaciofluvial) sediments are also incorporated within the moraines during pushing. For the first time, to our knowledge, we demonstrate categorically that these moraines formed sub‐annually using repeat uncrewed aerial vehicle (UAV) imagery. We present a conceptual model for sub‐annual moraine formation at Fjallsjökull that proposes the sawtooth moraine sequence comprises (i) sets of small squeeze moraines formed during melt‐driven squeeze events and (ii) larger push moraines formed during winter re‐advances. We suggest the development of this process‐form regime is linked to a combination of elevated temperatures, high surface meltwater fluxes to the bed, and emerging basal topography (a depositional overdeepening). These factors result in highly saturated subglacial sediments and high porewater pressures, which induces submarginal deformation and ice‐marginal squeezing during the melt season. Strong glacier recession during the summer, driven by elevated temperatures, allows several squeeze moraines to be emplaced. This process‐form regime may be characteristic of active temperate glaciers receding into overdeepenings during phases of elevated temperatures, especially where their englacial drainage systems allow efficient transfer of surface meltwater to the glacier bed near the snout margin

Normal X-inactivation mosaicism in corneas of heterozygous FlnaDilp2/+ female mice--a model of human Filamin A (FLNA) diseases

<p>Abstract</p> <p>Background</p> <p>Some abnormalities of mouse corneal epithelial maintenance can be identified by the atypical mosaic patterns they produce in X-chromosome inactivation mosaics and chimeras. Human <it>FLNA</it>/+ females, heterozygous for X-linked, filamin A gene (<it>FLNA</it>) mutations, display a range of disorders and X-inactivation mosaicism is sometimes quantitatively unbalanced. <it>Flna</it>^{<it>Dilp2/+ </it>}mice, heterozygous for an X-linked filamin A (<it>Flna</it>) nonsense mutation have variable eye, skeletal and other abnormalities, but X-inactivation mosaicism has not been investigated. The aim of this study was to determine whether X-inactivation mosaicism in the corneal epithelia of <it>Flna</it>^{<it>Dilp2/+ </it>}mice was affected in any way that might predict abnormal corneal epithelial maintenance.</p> <p>Results</p> <p>X-chromosome inactivation mosaicism was studied in the corneal epithelium and a control tissue (liver) of <it>Flna</it>^{<it>Dilp2/+ </it>}and wild-type (WT) female X-inactivation mosaics, hemizygous for the X-linked, <it>LacZ </it>reporter H253 transgene, using β-galactosidase histochemical staining. The corneal epithelia of <it>Flna</it>^{<it>Dilp2/+ </it>}and WT X-inactivation mosaics showed similar radial, striped patterns, implying epithelial cell movement was not disrupted in <it>Flna</it>^{<it>Dilp2/+ </it>}corneas. Corrected stripe numbers declined with age overall (but not significantly for either genotype individually), consistent with previous reports suggesting an age-related reduction in stem cell function. Corrected stripe numbers were not reduced in <it>Flna</it>^{<it>Dilp2/+ </it>}compared with WT X-inactivation mosaics and mosaicism was not significantly more unbalanced in the corneal epithelia or livers of <it>Flna</it>^{<it>Dilp2/+ </it>}than wild-type <it>Flna^+/+</it>X-inactivation mosaics.</p> <p>Conclusions</p> <p>Mosaic analysis identified no major effect of the mouse <it>Flna^Dilp2</it>mutation on corneal epithelial maintenance or the balance of X-inactivation mosaicism in the corneal epithelium or liver.</p

The electric wind of Venus: A global and persistent "polar wind"-like ambipolar electric field sufficient for the direct escape of heavy ionospheric ions

Understanding what processes govern atmospheric escape and the loss of planetary water is of paramount importance for understanding how life in the universe can exist. One mechanism thought to be important at all planets is an “ambipolar” electric field that helps ions overcome gravity. We report the discovery and first quantitative extraterrestrial measurements of such a field at the planet Venus. Unexpectedly, despite comparable gravity, we show the field to be five times stronger than in Earth's similar ionosphere. Contrary to our understanding, Venus would still lose heavy ions (including oxygen and all water-group species) to space, even if there were no stripping by the solar wind. We therefore find that it is possible for planets to lose heavy ions to space entirely through electric forces in their ionospheres and such an “electric wind” must be considered when studying the evolution and potential habitability of any planet in any star system

Lessons from mouse chimaera experiments with a reiterated transgene marker:revised marker criteria and a review of chimaera markers

Recent reports of a new generation of ubiquitous transgenic chimaera markers prompted us to consider the criteria used to evaluate new chimaera markers and develop more objective assessment methods. To investigate this experimentally we used several series of fetal and adult chimaeras, carrying an older, multi-copy transgenic marker. We used two additional independent markers and objective, quantitative criteria for cell selection and cell mixing to investigate quantitative and spatial aspects of developmental neutrality. We also suggest how the quantitative analysis we used could be simplified for future use with other markers. As a result, we recommend a five-step procedure for investigators to evaluate new chimaera markers based partly on criteria proposed previously but with a greater emphasis on examining the developmental neutrality of prospective new markers. These five steps comprise (1) review of published information, (2) evaluation of marker detection, (3) genetic crosses to check for effects on viability and growth, (4) comparisons of chimaeras with and without the marker and (5) analysis of chimaeras with both cell populations labelled. Finally, we review a number of different chimaera markers and evaluate them using the extended set of criteria. These comparisons indicate that, although the new generation of ubiquitous fluorescent markers are the best of those currently available and fulfil most of the criteria required of a chimaera marker, further work is required to determine whether they are developmentally neutral. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11248-015-9883-7) contains supplementary material, which is available to authorized users

A new class of hybrid secretion system is employed in Pseudomonas amyloid biogenesis

Gram-negative bacteria possess specialised biogenesis machineries that facilitate the export of amyloid subunits for construction of a biofilm matrix. The secretion of bacterial functional amyloid requires a bespoke outer-membrane protein channel through which unfolded amyloid substrates are translocated. Here, we combine X-ray crystallography, native mass spectrometry, single-channel electrical recording, molecular simulations and circular dichroism measurements to provide high-resolution structural insight into the functional amyloid transporter from Pseudomonas, FapF. FapF forms a trimer of gated β-barrel channels in which opening is regulated by a helical plug connected to an extended coil-coiled platform spanning the bacterial periplasm. Although FapF represents a unique type of secretion system, it shares mechanistic features with a diverse range of peptide translocation systems. Our findings highlight alternative strategies for handling and export of amyloid protein sequences

Fruit fracture biomechanics and the release of Lepidium didymum pericarp-imposed mechanical dormancy by fungi

Mechanical dormancy imposed by a hard fruit pericarp prevents premature seed germination. Here, the authors show that the pericarp of Lepidium didymum prevents germination by limiting water uptake and that dormancy can be released by fungal activity that weakens predetermined breaking zones in the fruit coat

Basonuclin-Null Mutation Impairs Homeostasis and Wound Repair in Mouse Corneal Epithelium

At least two cellular processes are required for corneal epithelium homeostasis and wound repair: cell proliferation and cell-cell adhesion. These processes are delicately balanced to ensure the maintenance of normal epithelial function. During wound healing, these processes must be reprogrammed in coordination to achieve a rapid re-epithelialization. Basonuclin (Bnc1) is a cell-type-specific transcription factor expressed mainly in the proliferative keratinocytes of stratified epithelium (e.g., corneal epithelium, epidermis and esophageal epithelium) and the gametogenic cells in testis and ovary. Our previous work suggested that basonuclin could regulate transcription of ribosomal RNA genes (rDNA) and genes involved in chromatin structure, transcription regulation, cell-cell junction/communication, ion-channels and intracelllular transportation. However, basonuclin's role in keratinocytes has not been demonstrated in vivo. Here we show that basonuclin-null mutation disrupts corneal epithelium homeostasis and delays wound healing by impairing cell proliferation. In basonuclin-null cornea epithelium, RNA polymerase I (Pol I) transcription is perturbed. This perturbation is unique because it affects transcripts from a subset of rDNA. Basonuclin-null mutation also perturbs RNA polymerase II (Pol II) transcripts from genes encoding chromatin structure proteins histone 3 and HMG2, transcription factor Gli2, gap-junction protein connexin 43 and adheren E-cadherin. In most cases, a concerted change in mRNA and protein level is observed. However, for E-cadherin, despite a notable increase in its mRNA level, its protein level was reduced. In conclusion, our study establishes basonuclin as a regulator of corneal epithelium homeostasis and maintenance. Basonuclin likely coordinates functions of a subset of ribosomal RNA genes (rDNA) and a group of protein coding genes in cellular processes critical for the regulation of cell proliferation

Amyloids - A functional coat for microorganisms

Amyloids are filamentous protein structures ~10 nm wide and 0.1–10 µm long that share a structural motif, the cross-β structure. These fibrils are usually associated with degenerative diseases in mammals. However, recent research has shown that these proteins are also expressed on bacterial and fungal cell surfaces. Microbial amyloids are important in mediating mechanical invasion of abiotic and biotic substrates. In animal hosts, evidence indicates that these protein structures also contribute to colonization by activating host proteases that are involved in haemostasis, inflammation and remodelling of the extracellular matrix. Activation of proteases by amyloids is also implicated in modulating blood coagulation, resulting in potentially life-threatening complications.