Foliar Morphology And Anatomy Of The Gigantopterid Plant Delnortea Abbottiae, From The Lower Permian Of West Texas

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142005/1/ajb214202.pd

Wei Hua's Four Parameter Potential Comments and Computation of Moleculer Constants \alpha_e and \omega_e x_e

The value of adjustable parameter $C$ and the four-parameter potential $U(r) = D_{e}\left [ \frac{1-{exp}[-b(r-r_{e})]}{1-C{exp} [-b(r-r_{e})]} \right ]^{2}$ has been expressed in terms of molecular parameters and its significance has been brought out. The potential so constructed, with $C$ derived from the molecular parameters, has been applied to ten electronic states in addition to the states studied by Wei Hua. Average mean deviation has been found to be 3.47 as compared to 6.93, 6.95 and 9.72 obtained from Levine2, Varshni and Morse potentials, respectively. Also Dunham's method has been used to express rotation-vibration interaction constant $(\alpha_{e})$ and anharmonocity constant $(\omega_{e}x_{e})$ in terms of $C$ and other molecular constants. These relations have been employed to determine these quantities for 37 electronic states. For $\alpha_{e}$, the average mean deviation is 7.2% compared to 19.7% for Lippincott's potential which is known to be the best to predict the values. Average mean deviation for $(\omega_{e}x_{e})$ turns out to be 17.4% which is almost the same as found from Lippincott's potential function.Comment: 19 RevTex Pages, 1 Ps figure, submitted to J. Phys.

WACCM-D Whole Atmosphere Community Climate Model with D-region ion chemistry

Energetic particle precipitation (EPP) and ion chemistry affect the neutral composition of the polar middle atmosphere. For example, production of odd nitrogen and odd hydrogen during strong events can decrease ozone by tens of percent. However, the standard ion chemistry parameterization used in atmospheric models neglects the effects on some important species, such as nitric acid. We present WACCM-D, a variant of the Whole Atmosphere Community Climate Model, which includes a set of lower ionosphere (D-region) chemistry: 307 reactions of 20 positive ions and 21 negative ions. We consider realistic ionization scenarios and compare the WACCM-D results to those from the Sodankylä Ion and Neutral Chemistry (SIC), a state-of-the-art 1-D model of the D-region chemistry. We show that WACCM-D produces well the main characteristics of the D-region ionosphere, as well as the overall proportion of important ion groups, in agreement with SIC. Comparison of ion concentrations shows that the WACCM-D bias is typically within ±10% or less below 70 km. At 70–90 km, when strong altitude gradients in ionization rates and/or ion concentrations exist, the bias can be larger for some groups but is still within tens of percent. Based on the good agreement overall and the fact that part of the differences are caused by different model setups, WACCM-D provides a state-of-the-art global representation of D-region ion chemistry and is therefore expected to improve EPP modeling considerably. These improvements are demonstrated in a companion paper by Andersson et al

Studies on the Restriction of Murine Leukemia Viruses by Mouse APOBEC3

APOBEC3 proteins function to restrict the replication of retroviruses. One mechanism of this restriction is deamination of cytidines to uridines in (−) strand DNA, resulting in hypermutation of guanosines to adenosines in viral (+) strands. However, Moloney murine leukemia virus (MoMLV) is partially resistant to restriction by mouse APOBEC3 (mA3) and virtually completely resistant to mA3-induced hypermutation. In contrast, the sequences of MLV genomes that are in mouse DNA suggest that they were susceptible to mA3-induced deamination when they infected the mouse germline. We tested the possibility that sensitivity to mA3 restriction and to deamination resides in the viral gag gene. We generated a chimeric MLV in which the gag gene was from an endogenous MLV in the mouse germline, while the remainder of the viral genome was from MoMLV. This chimera was fully infectious but its response to mA3 was indistinguishable from that of MoMLV. Thus, the Gag protein does not seem to control the sensitivity of MLVs to mA3. We also found that MLVs inactivated by mA3 do not synthesize viral DNA upon infection; thus mA3 restriction of MLV occurs before or at reverse transcription. In contrast, HIV-1 restricted by mA3 and MLVs restricted by human APOBEC3G do synthesize DNA; these DNAs exhibit APOBEC3-induced hypermutation

The Host Range of Gammaretroviruses and Gammaretroviral Vectors Includes Post-Mitotic Neural Cells

Gammaretroviruses and gammaretroviral vectors, in contrast to lentiviruses and lentiviral vectors, are reported to be restricted in their ability to infect growth-arrested cells. The block to this restriction has never been clearly defined. The original assessment of the inability of gammaretroviruses and gammaretroviral vectors to infect growth-arrested cells was carried out using established cell lines that had been growth-arrested by chemical means, and has been generalized to neurons, which are post-mitotic. We re-examined the capability of gammaretroviruses and their derived vectors to efficiently infect terminally differentiated neuroendocrine cells and primary cortical neurons, a target of both experimental and therapeutic interest.Using GFP expression as a marker for infection, we determined that both growth-arrested (NGF-differentiated) rat pheochromocytoma cells (PC12 cells) and primary rat cortical neurons could be efficiently transduced, and maintained long-term protein expression, after exposure to murine leukemia virus (MLV) and MLV-based retroviral vectors. Terminally differentiated PC12 cells transduced with a gammaretroviral vector encoding the anti-apoptotic protein Bcl-xL were protected from cell death induced by withdrawal of nerve growth factor (NGF), demonstrating gammaretroviral vector-mediated delivery and expression of genes at levels sufficient for therapeutic effect in non-dividing cells. Post-mitotic rat cortical neurons were also shown to be susceptible to transduction by murine replication-competent gammaretroviruses and gammaretroviral vectors.These findings suggest that the host range of gammaretroviruses includes post-mitotic and other growth-arrested cells in mammals, and have implications for re-direction of gammaretroviral gene therapy to neurological disease

The Gag Cleavage Product, p12, is a Functional Constituent of the Murine Leukemia Virus Pre-Integration Complex

The p12 protein is a cleavage product of the Gag precursor of the murine leukemia virus (MLV). Specific mutations in p12 have been described that affect early stages of infection, rendering the virus replication-defective. Such mutants showed normal generation of genomic DNA but no formation of circular forms, which are markers of nuclear entry by the viral DNA. This suggested that p12 may function in early stages of infection but the precise mechanism of p12 action is not known. To address the function and follow the intracellular localization of the wt p12 protein, we generated tagged p12 proteins in the context of a replication-competent virus, which allowed for the detection of p12 at early stages of infection by immunofluorescence. p12 was found to be distributed to discrete puncta, indicative of macromolecular complexes. These complexes were localized to the cytoplasm early after infection, and thereafter accumulated adjacent to mitotic chromosomes. This chromosomal accumulation was impaired for p12 proteins with a mutation that rendered the virus integration-defective. Immunofluorescence demonstrated that intracellular p12 complexes co-localized with capsid, a known constituent of the MLV pre-integration complex (PIC), and immunofluorescence combined with fluorescent in situ hybridization (FISH) revealed co-localization of the p12 proteins with the incoming reverse transcribed viral DNA. Interactions of p12 with the capsid and with the viral DNA were also demonstrated by co-immunoprecipitation. These results imply that p12 proteins are components of the MLV PIC. Furthermore, a large excess of wt PICs did not rescue the defect in integration of PICs derived from mutant p12 particles, demonstrating that p12 exerts its function as part of this complex. Altogether, these results imply that p12 proteins are constituent of the MLV PIC and function in directing the PIC from the cytoplasm towards integration