Three-Nucleon Force Effects in Nucleon Induced Deuteron Breakup: Predictions of Current Models (I)

An extensive study of three-nucleon force effects in the entire phase space of the nucleon-deuteron breakup process, for energies from above the deuteron breakup threshold up to 200 MeV, has been performed. 3N Faddeev equations have been solved rigorously using the modern high precision nucleon-nucleon potentials AV18, CD Bonn, Nijm I, II and Nijm 93, and also adding 3N forces. We compare predictions for cross sections and various polarization observables when NN forces are used alone or when the two pion-exchange Tucson-Melbourne 3NF was combined with each of them. In addition AV18 was combined with the Urbana IX 3NF and CD Bonn with the TM' 3NF, which is a modified version of the TM 3NF, more consistent with chiral symmetry. Large but generally model dependent 3NF effects have been found in certain breakup configurations, especially at the higher energies, both for cross sections and spin observables. These results demonstrate the usefulness of the kinematically complete breakup reaction in testing the proper structure of 3N forces.Comment: 42 pages, 20 ps figures, 2 gif figure

Quantum dynamics of molecules in 4He nano-droplets: Microscopic Superfluidity

High resolution spectroscopy of doped molecules in 4He nano-droplets and clusters gives a signature of superfluidity in microscopic system, termed as microscopic superfluidity. Ro-vibrational spectrum of 4HeN-M clusters is studied with the help of some important observations, revealed from experiments (viz., localised and orderly arrangement of 4He atoms, although, being free to move in the order of their locations; individual 4He atoms can not be tagged as normal/ superfluid, etc.) and other factors (e.g., consideration that the 4He atoms which happen to fall in the plane of rotation of a molecule, render a equipotential ring and thus, do not take part in rotation; etc.) which effect the rotational and vibrational spectrum of the system. This helps us in successfully explaining the experimental findings which state that the rotational spectrum of clusters have sharp peaks (indicating that the molecule rotates like a free rotor) and moment of inertia and vibrational frequency shift have a non-trivial dependence on N

Spare PRELI Gene Loci: Failsafe Chromosome Insurance?

LEA (late embryogenesis abundant) proteins encode conserved N-terminal mitochondrial signal domains and C-terminal (A/TAEKAK) motif repeats, long-presumed to confer cell resistance to stress and death cues. This prompted the hypothesis that LEA proteins are central to mitochondria mechanisms that connect bioenergetics with cell responses to stress and death signaling. In support of this hypothesis, recent studies have demonstrated that mammalian LEA protein PRELI can act as a biochemical hub, which upholds mitochondria energy metabolism, while concomitantly promoting B cell resistance to stress and induced death. Hence, it is important to define in vivo the physiological relevance of PRELI expression.Given the ubiquitous PRELI expression during mouse development, embryo lethality could be anticipated. Thus, conditional gene targeting was engineered by insertion of flanking loxP (flox)/Cre recognition sites on PRELI chromosome 13 (Chr 13) locus to abort its expression in a tissue-specific manner. After obtaining mouse lines with homozygous PRELI floxed alleles (PRELI(f/f)), the animals were crossed with CD19-driven Cre-recombinase transgenic mice to investigate whether PRELI inactivation could affect B-lymphocyte physiology and survival. Mice with homozygous B cell-specific PRELI deletion (CD19-Cre/Chr13 PRELI(-/-)) bred normally and did not show any signs of morbidity. Histopathology and flow cytometry analyses revealed that cell lineage identity, morphology, and viability were indistinguishable between wild type CD19-Cre/Chr13 PRELI(+/+) and CD19-Cre/Chr13 PRELI(-/-) deficient mice. Furthermore, B cell PRELI gene expression seemed unaffected by Chr13 PRELI gene targeting. However, identification of additional PRELI loci in mouse Chr1 and Chr5 provided an explanation for the paradox between LEA-dependent cytoprotection and the seemingly futile consequences of Chr 13 PRELI gene inactivation. Importantly, PRELI expression from spare gene loci appeared ample to surmount Chr 13 PRELI gene deficiency.These findings suggest that PRELI is a vital LEA B cell protein with failsafe genetics

Transcriptome analysis of complex I-deficient patients reveals distinct expression programs for subunits and assembly factors of the oxidative phosphorylation system

Contains fulltext : 154334.pdf (publisher's version ) (Open Access)BACKGROUND: Transcriptional control of mitochondrial metabolism is essential for cellular function. A better understanding of this process will aid the elucidation of mitochondrial disorders, in particular of the many genetically unsolved cases of oxidative phosphorylation (OXPHOS) deficiency. Yet, to date only few studies have investigated nuclear gene regulation in the context of OXPHOS deficiency. In this study we performed RNA sequencing of two control and two complex I-deficient patient cell lines cultured in the presence of compounds that perturb mitochondrial metabolism: chloramphenicol, AICAR, or resveratrol. We combined this with a comprehensive analysis of mitochondrial and nuclear gene expression patterns, co-expression calculations and transcription factor binding sites. RESULTS: Our analyses show that subsets of mitochondrial OXPHOS genes respond opposingly to chloramphenicol and AICAR, whereas the response of nuclear OXPHOS genes is less consistent between cell lines and treatments. Across all samples nuclear OXPHOS genes have a significantly higher co-expression with each other than with other genes, including those encoding mitochondrial proteins. We found no evidence for complex-specific mRNA expression regulation: subunits of different OXPHOS complexes are similarly (co-)expressed and regulated by a common set of transcription factors. However, we did observe significant differences between the expression of nuclear genes for OXPHOS subunits versus assembly factors, suggesting divergent transcription programs. Furthermore, complex I co-expression calculations identified 684 genes with a likely role in OXPHOS biogenesis and function. Analysis of evolutionarily conserved transcription factor binding sites in the promoters of these genes revealed almost all known OXPHOS regulators (including GABP, NRF1/2, SP1, YY1, E-box factors) and a set of novel candidates (ELK1, KLF7, SP4, EHF, ZNF143, and TEL2). CONCLUSIONS: OXPHOS genes share an expression program distinct from other genes encoding mitochondrial proteins, indicative of targeted nuclear regulation of a mitochondrial sub-process. Within the subset of OXPHOS genes we established a difference in expression between mitochondrial and nuclear genes, and between nuclear genes encoding subunits and assembly factors. Most transcription regulators of genes that co-express with complex I are well-established factors for OXPHOS biogenesis. For the remaining six factors we here suggest for the first time a link with transcription regulation in OXPHOS deficiency