The genome of the extremophile crucifer Thellungiella parvula

Thellungiella parvula is related to Arabidopsis thaliana and is endemic to saline, resource-poor habitats, making it a model for the evolution of plant adaptation to extreme environments. Here we present the draft genome for this extremophile species. Exclusively by next generation sequencing, we obtained the de novo assembled genome in 1,496 gap-free contigs, closely approximating the estimated genome size of 140 Mb. We anchored these contigs to seven pseudo chromosomes without the use of maps. We show that short reads can be assembled to a near-complete chromosome level for a eukaryotic species lacking prior genetic information. The sequence identifies a number of tandem duplications that, by the nature of the duplicated genes, suggest a possible basis for T. parvula's extremophile lifestyle. Our results provide essential background for developing genomically influenced testable hypotheses for the evolution of environmental stress tolerance.     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.     

Systemic Research Practices Towards the Development of an Eco-Community in Vietnam: some Joint Post-Facto Reflections

In this article we discuss how an interdisciplinary research team partnered with a variety of stakeholders concerned with and/or affected by the impacts of climate change in the Red River Delta of Vietnam. The research, undertaken from 2016 to 2018, drew upon a wide range of methods to investigate systemically these impacts – with a view to the research inputting into the development of (more) sustainable ways of living. The research solicited various accounts of the experience of climate change in the community, set up learning processes in community meetings, and created an interface with government officials positioned at commune, district, provincial, and national levels. The intention was to offer support towards developing a learning process (broadly defined as including learnings/systemic inquiry across organizational levels of the society) to pursue options for sustainable living. The article offers our post-facto reflections which render more explicit (to ourselves and for the benefit of audiences) how the research team, with Hoang as lead researcher, facilitated the inquiry process towards developing a synthesis which underscored the assets for resilience to climate change and supported interventions to strengthen such (defined) assets.

     

DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1

A single double-strand break (DSB) induced by HO endonuclease triggers both repair by homologous recombination and activation of the Mec1-dependent DNA damage checkpoint in budding yeast. Here we report that DNA damage checkpoint activation by a DSB requires the cyclin-dependent kinase CDK1 (Cdc28) in budding yeast. CDK1 is also required for DSB-induced homologous recombination at any cell cycle stage. Inhibition of homologous recombination by using an analogue-sensitive CDK1 protein results in a compensatory increase in non-homologous end joining. CDK1 is required for efficient 5' to 3' resection of DSB ends and for the recruitment of both the single-stranded DNA-binding complex, RPA, and the Rad51 recombination protein. In contrast, Mre11 protein, part of the MRX complex, accumulates at unresected DSB ends. CDK1 is not required when the DNA damage checkpoint is initiated by lesions that are processed by nucleotide excision repair. Maintenance of the DSB-induced checkpoint requires continuing CDK1 activity that ensures continuing end resection. CDK1 is also important for a later step in homologous recombination, after strand invasion and before the initiation of new DNA synthesis.     

本溪地区BIF中玄武质围岩的高场强元素特征

辽宁本溪地区条带状铁矿(BIF)与其玄武质火山围岩之间的时空关联非常密切.对于玄武质火山围岩高场强元素(HFSE)的研究表明:wNb/wTa比值(7.00~19.93)表现出明显的分异,而wZr/wHf比值(33.46~38.28)则变化不大;从弓长岭到南芬、歪头山样品的wNb/wTa比值变化具有明显的循序性.这种高场强元素的迁移和分异特征反映出俯冲作用与盆地演化之间的关联.研究区玄武质火山围岩(wNb/wYb)N比值大于1(1.21~18.45,平均2.72),这进一步表明,其形成的构造背景为陆内弧后盆地提供了有利于BIF形成的条件.     

基于热压块的不锈钢粉尘还原实验

为了从不锈钢粉尘中回收利用Fe,Cr和Ni等,对不锈钢粉尘热压块制备及其自还原过程进行了研究.在热压温度为200℃,热压压力为35 MPa条件下,抗压强度达到900 N/个以上.高温条件下,煤热解产生的挥发分可参与不锈钢粉尘还原反应,当还原温度为1 400,1 450℃时,挥发分还原作用率达到0.4.据XRD分析和热力学计算,自还原过程中含铬物质的物相转变顺序为Fe Cr2O4,Cr2O3,Cr7C3,[Cr]Fe-Cr-Ni-C.当还原温度为1 450℃,烟煤中固定碳与粉尘中可去除氧的物质量的比(xc/xo)为0.72时,不锈钢粉尘热压块不能完全还原;当xc/xo大于0.8,还原20 min时,不锈钢粉尘热压块能完全还原.