Transcription profiles of mitochondrial genes correlate with mitochondrial DNA haplotypes in a natural population of Silene vulgaris

<p>Abstract</p> <p>Background</p> <p>Although rapid changes in copy number and gene order are common within plant mitochondrial genomes, associated patterns of gene transcription are underinvestigated. Previous studies have shown that the gynodioecious plant species <it>Silene vulgaris </it>exhibits high mitochondrial diversity and occasional paternal inheritance of mitochondrial markers. Here we address whether variation in DNA molecular markers is correlated with variation in transcription of mitochondrial genes in <it>S. vulgaris </it>collected from natural populations.</p> <p>Results</p> <p>We analyzed RFLP variation in two mitochondrial genes, <it>cox1 </it>and <it>atp1</it>, in offspring of ten plants from a natural population of <it>S. vulgaris </it>in Central Europe. We also investigated transcription profiles of the <it>atp1 </it>and <it>cox1 </it>genes. Most DNA haplotypes and transcription profiles were maternally inherited; for these, transcription profiles were associated with specific mitochondrial DNA haplotypes. One individual exhibited a pattern consistent with paternal inheritance of mitochondrial DNA; this individual exhibited a transcription profile suggestive of paternal but inconsistent with maternal inheritance. We found no associations between gender and transcript profiles.</p> <p>Conclusions</p> <p>Specific transcription profiles of mitochondrial genes were associated with specific mitochondrial DNA haplotypes in a natural population of a gynodioecious species <it>S. vulgaris</it>.</p> <p>Our findings suggest the potential for a causal association between rearrangements in the plant mt genome and transcription product variation.</p

A poxvirus pseudokinase represses viral DNA replication via a pathway antagonized by its paralog kinase

Poxviruses employ sophisticated, but incompletely understood, signaling pathways that engage cellular defense mechanisms and simultaneously ensure viral factors are modulated properly. For example, the vaccinia B1 protein kinase plays a vital role in inactivating the cellular antiviral factor BAF, and likely orchestrates other pathways as well. In this study, we utilized experimental evolution of a B1 deletion virus to perform an unbiased search for suppressor mutations and identify novel pathways involving B1. After several passages of the ΔB1 virus we observed a robust increase in viral titer of the adapted virus. Interestingly, our characterization of the adapted viruses reveals that mutations correlating with a loss of function of the vaccinia B12 pseudokinase provide a striking fitness enhancement to this virus. In support of predictions that reductive evolution is a driver of poxvirus adaptation, this is clear experimental evidence that gene loss can be of significant benefit. Next, we present multiple lines of evidence demonstrating that expression of full length B12 leads to a fitness reduction in viruses with a defect in B1, but has no apparent impact on wild-type virus or other mutant poxviruses. From these data we infer that B12 possesses a potent inhibitory activity that can be masked by the presence of the B1 kinase. Further investigation of B12 attributes revealed that it primarily localizes to the nucleus, a characteristic only rarely found among poxviral proteins. Surprisingly, BAF phosphorylation is reduced under conditions in which B12 is present in infected cells without B1, indicating that B12 may function in part by enhancing antiviral activity of BAF. Together, our studies of B1 and B12 present novel evidence that a paralogous kinase-pseudokinase pair can exhibit a unique epistatic relationship in a virus, perhaps serving to enhance B1 conservation during poxvirus evolution and to orchestrate yet-to-be-discovered nuclear events during infection

Cold atom confinement in an all-optical dark ring trap

We demonstrate confinement of $^{85}$Rb atoms in a dark, toroidal optical trap. We use a spatial light modulator to convert a single blue-detuned Gaussian laser beam to a superposition of Laguerre-Gaussian modes that forms a ring-shaped intensity null bounded harmonically in all directions. We measure a 1/e spin-relaxation lifetime of ~1.5 seconds for a trap detuning of 4.0 nm. For smaller detunings, a time-dependent relaxation rate is observed. We use these relaxation rate measurements and imaging diagnostics to optimize trap alignment in a programmable manner with the modulator. The results are compared with numerical simulations.Comment: 5 pages, 4 figure

Collecting genetic material from beef cattle (2005)

The beef cattle industry has long awaited the development of genetic tests to assist producers in breeding selection and management and to improve the marketability of cattle. Currently, there are only a handful of genetic tests commercially available for beef cattle. Beef producers interested in using genetic testing to improve their breeding stock need to know how to collect and store various genetic materials for testing.New February 2005 -- Extension website

The Vaccinia Virus (VACV) B1 and Cellular VRK2 Kinases Promote VACV Replication Factory Formation through Phosphorylation-Dependent Inhibition of VACV B12

Comparative examination of viral and host protein homologs reveals novel mechanisms governing downstream signaling effectors of both cellular and vi- ral origin. The vaccinia virus B1 protein kinase is involved in promoting multiple facets of the virus life cycle and is a homolog of three conserved cellular enzymes called vaccinia virus-related kinases (VRKs). Recent evidence indicates that B1 and VRK2 mediate a com- mon pathway that is largely uncharacterized but appears independent of previous VRK substrates. Interestingly, separate studies described a novel role for B1 in inhibiting vac- cinia virus protein B12, which otherwise impedes an early event in the viral lifecycle. Herein, we characterize the B1/VRK2 signaling axis to better understand their shared functions. First, we demonstrate that vaccinia virus uniquely requires VRK2 for viral repli- cation in the absence of B1, unlike other DNA viruses. Employing loss-of-function analy- sis, we demonstrate that vaccinia virus’s dependence on VRK2 is only observed in the presence of B12, suggesting that B1 and VRK2 share a pathway controlling B12. More- over, we substantiate a B1/VRK2/B12 signaling axis by examining coprecipitation of B12 by B1 and VRK2. Employing execution point analysis, we reveal that virus replication proceeds normally through early protein translation and uncoating but stalls at replica- tion factory formation in the presence of B12 activity. Finally, structure/function analyses of B1 and VRK2 demonstrate that enzymatic activity is essential for B1 or VRK2 to inhibit B12. Together, these data provide novel insights into B1/VRK signaling coregulation and support a model in which these enzymes modulate B12 in a phosphorylation-depen- dent manner

Asymmetrical crossing barriers in angiosperms

Patterns of reproductive isolation between species may provide insight into the mechanisms and evolution of barriers to interspeci¢c gene exchange. We used data from published interspeci¢c hybridization experiments from 14 genera of angiosperms in order to test for the presence of asymmetrical barriers to gene exchange. Reproductive isolation was examined at three life-history stages: the ability of interspeci¢c crosses to produce seeds, the viability of F 1 hybrids, and the fertility of F 1 hybrids. Statistically signi¢cant asymmetries in the strength of reproductive isolation between species were detected in all genera and at each of the three life-history stages. Asymmetries in seed production may be caused by a variety of mechanisms including di¡erences in stigma/style lengths, self compatibility and di¡erential fruit abortion. Asymmetries in post-zygotic isolation are probably caused by nuclear^cytoplasmic interactions. Asymmetrical reproductive isolation between plant taxa may have important implications for the dynamics of hybrid zones, the direction of genetic introgression and the probability of reinforcement

Evolutionary fates within a microbial population highlight an essential role for protein folding during natural selection

Physicochemical properties of molecules can be linked directly to evolutionary fates of a population in a quantitative and predictive manner.Reversible- and irreversible-folding pathways must be accounted for to accurately determine in vitro kinetic parameters (KM and kcat) at temperatures or conditions in which a significant fraction of free enzyme is unfolded.In vivo population dynamics can be reproduced using in vitro physicochemical measurements within a model that imposes an activity threshold above which there is no added fitness benefit

A High-Rate, Heterogeneous Data Set from the Darpa Urban Challenge

This paper describes a data set collected by MIT’s autonomous vehicle Talos during the 2007 DARPA Urban Challenge. Data from a high-precision navigation system, five cameras, 12 SICK planar laser range scanners, and a Velodyne high-density laser range scanner were synchronized and logged to disk for 90 km of travel. In addition to documenting a number of large loop closures useful for developing mapping and localization algorithms, this data set also records the first robotic traffic jam and two autonomous vehicle collisions. It is our hope that this data set will be useful to the autonomous vehicle community, especially those developing robotic perception capabilities.United States. Defense Advanced Research Projects Agency (Urban Challenge, ARPA Order No. W369/00, Program Code DIRO, issued by DARPA/CMO under Contract No. HR0011-06-C-0149

Vaccinia Virus Arrests and Shifts the Cell Cycle

Modulation of the host cell cycle is a common strategy used by viruses to create a proreplicative environment. To facilitate viral genome replication, vaccinia virus (VACV) has been reported to alter cell cycle regulation and trigger the host cell DNA damage response. However, the cellular factors and viral effectors that mediate these changes remain unknown. Here, we set out to investigate the effect of VACV infection on cell proliferation and host cell cycle progression. Using a subset of VACV mutants, we characterise the stage of infection required for inhibition of cell proliferation and define the viral effectors required to dysregulate the host cell cycle. Consistent with previous studies, we show that VACV inhibits and subsequently shifts the host cell cycle. We demonstrate that these two phenomena are independent of one another, with viral early genes being responsible for cell cycle inhibition, and post-replicative viral gene(s) responsible for the cell cycle shift. Extending previous findings, we show that the viral kinase F10 is required to activate the DNA damage checkpoint and that the viral B1 kinase and/or B12 pseudokinase mediate degradation of checkpoint effectors p53 and p21 during infection. We conclude that VACV modulates host cell proliferation and host cell cycle progression through temporal expression of multiple VACV effector proteins. (209/200.