112,510 research outputs found
Spiral Structure in Galaxies : A Density Wave Theory
No full textHow does it happen that billions of stars can cooperate to produce the beautiful spirals that characterize so many galaxies, including ours? This book presents a theory of spiral structure that has been developed over the past three decades under the continuous stimulus of new observational studies. The theory unfolds in a way that can be grasped by any reader with an undergraduate science background who is interested in astronomy, as well as by graduate students and scientists actively involved in astronomy or related subjects who want to see the "backbone" and the physical content of the theory. The foundations of this theoretical framework were laid in the early 1960s, following the pioneering work of B. Lindblad. C. C. Lin had already contributed significantly to the field of fluid mechanics when he turned his attention to spiral structures, and he has focused on the problem ever since. Giuseppe Bertin joined this research effort when he first visited at MIT in 1975, bringing to the project knowledge from his work on elliptical galaxies and plasma astrophysics. Together, Bertin and Lin have contributed to the exciting developments on spiral structure of the last few decades, working closely with many observers and other theorists. In this book they describe the density-wave theory with the goal of making the key concepts and astrophysical implications explicit and accessible. The essence of the solution Bertin and Lin present is that the spirals are wave rather than material phenomena and generally trace intrinsic characteristics of the individual galaxies. The book is in three parts—Physical Concepts, Observational Studies, and Dynamical Mechanisms—with most of the technical details confined to the last part
Mammalian LIN-7 PDZ proteins associate with beta-catenin at the cell junctions of epithelia and neurons
No full textThe heterotrimeric PDZ complex containing LIN-2, LIN-7 and LIN-10 is known to be involved in the organization of epithelial and neuronal junctions in Caenorhabditis elegans and mammals. We report here that mammalian LIN-7 PDZ proteins form a complex with cadherin and β-catenin in epithelia and neurons. The association of LIN-7 with cadherin and β-catenin is Ca2+ dependent and is mediated by the direct binding of LIN-7 to the C-terminal PDZ target sequence of β-catenin, as demonstrated by means of co-immunoprecipitation experiments and in vitro binding assays with the recombinant glutathione S-transferase:LIN-7A. The presence of β-catenin at the junction is required in order to relocate LIN-7 from the cytosol to cadherin-mediated adhesions, thus indicating that LIN-7 junctional recruitment is β-catenin dependent and that one functional role of the binding is to localize LIN-7. Moreover, when LIN-7 is present at the β-catenin-containing junctions, it determines the accumulation of binding partners, thus suggesting the mechanism by which β-catenin mediates the organization of the junctional domai
LIN-2/CASK binds to both ACR-16 and UNC-29 through SH3 domain.
No full text(A) Summary of interactions by Yeast two-hybrid. Strong interaction (++); weak interaction (+), and no interactions (-) were indicated. (B) LIN-2A’s SH3 domain binds the ACR-16’s second intracellular loop (LoopII) in a Yeast two-hybrid assay. Y2HGold cells carrying indicated plasmids (Left) growing on selective media (-Trp/-Leu/-His/-Ade) is shown (Right). (C) LIN-2A’s SH3 domain binds the UNC-29’s second intracellular loop (LoopII) in the Yeast two-hybrid assay. (D-E) FRM-3 do not bind the ACR-16’s second intracellular loop (LoopII) (D) and UNC-29’s second intracellular loop (LoopII) (E) in the Yeast two-hybrid assay. (F-G) LIN-2A binds FRM-3 (F) and its FERM domain (G) requiring its PDZ domain, but not SH3 domain.</p
Evolution of the G+C content frontier in the rat cytomegalovirus genome
No full textWithin the 230138 bp of the rat cytomegalovirus (RCMV) genome, the G+C content changes abruptly at position 142644, constituting a G+C content frontier. To the left of this point, overall G+C content is 69.2%, and to the right it is only 47.6%. A region of extremely low G+C content (33.8%) is found in the 5 kb immediately to the right of the frontier, in which there are no predicted coding sequences. To the right of position 147501, the G+C content rises and predicted coding sequences reappear. However, these genes are much shorter (average 848bp, 50% G+C) than those in the left two-thirds of the genome (average 1462bp, 70% G+C). Whole genome alignment of several viruses indicates that the initial ultra-low G+C region appeared in the common ancestor of the genera Cytomegalovirus and Muromegalovirus, and that the lowering of G+C in the right third has been a subsequent process in the lineage leading to RCMV. The left two-thirds of RCMV has stop codon occurrences at 67.5% of their expected level, based on a modified Markov chain model of stop codon distribution, and the corresponding figure for the right third is 78%. Therefore, despite heavy mutation pressure, selective constraint has operated in the right third of the RCMV genome to maintain a degree of gene length unusual for such low G+C sequences
The Cold Shock Domain Protein LIN-28 Controls Developmental Timing in C. elegans and Is Regulated by the lin-4 RNA
No full textAbstractMutations in the heterochronic gene lin-28 of C. elegans cause precocious development where diverse events specific to the second larval stage are skipped. lin-28 encodes a cytoplasmic protein with a cold shock domain and retroviral-type (CCHC) zinc finger motifs, consistent with a role for LIN-28 in posttranscriptional regulation. The 3′UTR of lin-28 contains a conserved element that is complementary to the 22 nt regulatory RNA product of lin-4 and that resembles seven such elements in the 3′UTR of the heterochronic gene lin-14. Both lin-4 activity and the lin-4-complementary element (LCE) are necessary for stage-specific regulation of lin-28. Deleting the LCE produces a dominant gain-of-function allele that causes a retarded phenotype, indicating that lin-28 activity is a switch that controls choices of stage-specific fates
Differential roles of the microRNA let-7 in C. elegans tissue development
No full textThe organs and tissues of the human body comprise of an astonishing variety of cells as different in morphology and function as muscle cells and neurons. Amazingly, despite their different protein contents, they largely contain the identical genomic information. In order to understand the processes that enable this differentiation, we need to determine the underlying regulatory mechanisms. A very recent discovery in this context was the posttranscriptional regulation of gene expression by microRNAs (miRNAs). miRNAs are small RNA molecules that mediate translational repression and degradation of mRNA transcripts through partial complementarity to their 3’ untranslated region (UTR) . Among the first miRNAs to be identified, let-7 stands out for its high conservation in sequence and developmental functions in development throughout the animal kingdom. During my PhD, I studied the role of let-7 in Caenorhabditis elegans in the context of two distinct processes of tissue development, namely differentiation of the epidermis (called hypodermis), and morphogenesis of the vulva. The functions of the let-7 miRNA in formation of the adult cuticle have been extensively studied and are well understood. let-7 controls differentiation of specific, mitotically active epidermal cells by inducing cell cycle exit, fusion, and switch to an adult specific transcriptional program upon repression of targets such as lin-41, daf-12, hbl-1 and let-60/ras. I set out to identify novel interactors of let-7 in a genome-wide RNAi screen for suppression of the lethal let-7 bursting phenotype. Candidates were then verified using fluorescence-based reporter systems for onset of hypodermis differentiation and intensity of repression of a known target. Thereby, I was able to validate a whole set of novel members of the let-7 network, comprising genes downstream in the pathway as well as potential regulators of let-7 activity. Notably, both groups of repressors contain factors required for cell cycle progression and mitosis, which indicates an active crosstalk between let-7 and the cell-cycle machinery. In a second project, I explored the molecular basis for the prominent let-7 vulval bursting phenotype. Despite the absence of overproliferation or any other obvious phenotype in vulval morphogenesis, I was able to show that let-7 activity is required in the vulva, and that its major function in this context is repression of a single target, namely lin-41. Disruption of let-7 binding to lin-41 through modification of the let-7 complementary sites by CRISPR/Cas9 mediated genome editing suffices to trigger the bursting phenotype, proving that repression of a single target is the key function of the miRNA in this context. In summary, my work shows that while both differentiation of hypodermis as well as vulval integrity are mediated through repression of lin-41, the downstream effect of this regulation seem to differ, suggesting that let-7 can be wired to control distinct processes depending on the cellular context. With respect to the latest findings both in C. elegans as well as in mammals, it will be interesting to determine if this depends on differential molecular functions of LIN-41 in the two tissues
Spatial Chow-Lin Methods for Data Completion in Econometric Flow Models
No full textFlow data across regions can be modeled by spatial econometric models, see LeSage and Pace (2009). Recently, regional studies became interested in the aggregation and disaggregation of flow models, because trade data cannot be obtained at a disaggregated level but data are published on an aggregate level. Furthermore, missing data in disaggregated flow models occur quite often since detailed measurements are often not possible at all observation points in time and space. In this paper we develop classical and Bayesian methods to complete flow data. The Chow and Lin (1971) method was developed for completing disaggregated incomplete time series data. We will extend this method in a general framework to spatially correlated flow data using the cross-sectional Chow-Lin method of Polasek et al. (2009). The missing disaggregated data can be obtained either by feasible GLS prediction or by a Bayesian (posterior) predictive density.Missing values in spatial econometrics, MCMC, non-spatial Chow-Lin (CL) and spatial Chow-Lin (SCL) methods, spatial internal flow (SIF) models, origin and destination (OD) data
LIN-2 and FRM-3 regulate the synaptic abundance but not surface expression level of AChRs.
No full text(A-D) ACR-16::RFP and UNC-29::RFP synaptic abundance were decreased in lin-2null and frm-3null mutants. Representative images (A, C, scale bar 10 μm) and mean puncta intensity (B, D) are shown. The wild type is normalized to 1. (E-H) ACh- and Levamisole-activated currents were unaltered in lin-2null and frm-3null mutants. Representative traces (E, G) and mean current amplitude (F, H) are shown. (I, J) GABA-activated currents were decreased by 50% in lin-2null mutants but were unchanged in frm-3null mutants. Data are mean ± SEM (***, p < 0.001 when compared to control; one-way ANOVA). The number of worms analyzed for each genotype is indicated in the bar.</p
Identification of cis-regulatory elements from the C. elegans Hox gene lin-39 required for embryonic expression and for regulation by the transcription factors LIN-1, LIN-31 and LIN-39
No full textExpression of the Caenorhabditis elegans Hox gene lin-39 begins in the embryo and continues in multiple larval cells, including the P cell lineages that generate ventral cord neurons (VCNs) and vulval precursor cells (VPCs). lin-39 is regulated by several factors and by Wnt and Ras signaling pathways; however, no cis-acting sites mediating lin-39 regulation have been identified. Here, we describe three elements controlling lin-39 expression: a 338-bp upstream fragment that directs embryonic expression in P5-P8 and their descendants in the larva, a 247-bp intronic region sufficient for VCN expression, and a 1.3-kb upstream cis-regulatory module that drives expression in the VPC P6.p in a Ras-dependent manner. Three trans-acting factors regulate expression via the 1.3-kb element. A single binding site for the ETS factor LIN-1 mediates repression in VPCs other than P6.p; however, loss of LIN-1 decreases expression in P6.p. Therefore, LIN-1 acts both negatively and positively on lin-39 in different VPCs. The Forkhead domain protein LIN-31 also acts positively on lin-39 in P6.p via this module. Finally, LIN-39 itself binds to this element, suggesting that LIN-39 autoregulates its expression in P6.p. Therefore, we have begun to unravel the cis-acting sites regulating lin-39 Hox gene expression and have shown that lin-39 is a direct target of the Ras pathway acting via LIN-1 and LIN-31..SC: 0S; 7B; 0T; CA; PE; EC; SO; AA; XURL: URL; E-MAIL; DOI; DIGITAL-OBJECT-IDENTIFIERSource type: Electronic(1)[email protected]; http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WDG-4K0C9JV-3&_user=10&_coverDate=09%2F15%2F2006&_rdoc=21&_fmt=summary&_orig=browse&_srch=doc-info(%23toc%236766%232006%23997029997%23633147%23FLA%23display%23Volume)&_cdi=6766&_sort=d&_docanchor=&view=c&_ct=24&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3e6063983fd5b459eac74b274375875e; http://upei-resolver.asin-risa.ca?sid=SP:CABI&id=pmid:&id=doi%3a10.1016%2fj.ydbio.2006.05.008&issn=0012-1606&isbn=&volume=297&issue=2&spage=550&pages=550-565&date=2006&title=Developmental%20Biology&atitle=Identification%20of%20cis-regulatory%20elements%20from%20the%20C.%20elegans%20Hox%20gene%20lin-39%20required%20for%20embryonic%20expression%20and%20for%20regulation%20by%20the%20transcription%20factors%20LIN-1%2c%20LIN-31%20and%20LIN-39.&aulast=Wagmaister&pid=%3Cauthor%3EWagmaister%2c%20J%20A%3bMiley%2c%20G%20R%3bMorris%2c%20C%20A%3bGleason%2c%20J%20E%3bMiller%2c%20L%20M%3bKornfeld%2c%20K%3bEisenmann%2c%20D%20M%3C%2Fauthor%3E%3CAN%3E20073040429%3C%2FAN%3E%3CDT%3EJournal%20article%3C%2FDT%3
Rathalos treecko Lin & Zhao & Koh & Li 2022, comb. nov.
No full textRathalos treecko (Lin & Li, 2021) comb. nov. Anyphaena treecko Lin & Li, In: Lin et al., 2021: 101, figs 9A–C, 10A–B, 14I–J. Material examined. Holotype ♂ (IZCAS-Ar42404), China: Hainan, Changjiang County, Bawangling, Dongsizhan (19.0495°N, 109.1157°E), 23 April 2009, G. Tang leg. (examined). Paratypes. 2♀ (IZCAS-Ar42405–Ar42406), same data as holotype (examined). Diagnosis. See Lin et al. (2021). Description. See Lin et al. (2021). Distribution. China (Hainan). Comments. The cymbial apophysis, the triangular epigyne and the straight copulatory duct indicate that this species belongs to Rathalos Lin & Li, gen. nov. Thus, we transfer it from Anyphaena to Rathalos Lin & Li, gen. nov.Published as part of Lin, Yejie, Zhao, Huifeng, Koh, Joseph K H & Li, Shuqiang, 2022, Taxonomy notes on twenty-eight spider species (Arachnida: Araneae) from Asia, pp. 198-270 in Zoological Systematics 47 (3) on page 201, DOI: 10.11865/zs.2022303, http://zenodo.org/record/717585
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