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Motivation: In spite of a well-known fact that genome rearrangements are supposed to be viewed in the light of the evolutionary relationships within and between the species involved, no formal underlying framework based on the evolutionary considerations for treating the questions arising in the area has been proposed. If such an underlying framework is provided, all the basic questions in the area can be posed in a biologically more appropriate and useful form: e.g., the similarity between two genomes can then be computed via the nearest ancestor, rather than 'directly', ignoring the evolutionary connections.
Results: We outline an evolution-based general framework for answering questions related to the multiple genome rearrangement. In the proposed model, the evolutionary genome graph (EG-graph) encapsulates an evolutionary history of a genome family. For a set of all EG-graphs, we introduce a family of similarity measures, each defined via a fixed set of genome transformations. Given a set of genomes and restricting ourselves to the transpositions, an algorithm for constructing an EG-graph is presented. We also present the experimental results in the form of an EG-graph for a set of concrete genomes (for several species). This EG-graph turns out to be very close to the corresponding known phylogenetic tree.
Contact: dkorkin@unb.ca
Keywords: genome rearrangement; evolutionary model; gene transformations; longest common subsequence; ETS framework.

The rate coefficient for the reaction O + ClO → Cl + O2 (1) was measured over the range 227 to 362 K using a discharge flow tube coupled to a pulsed laser photolysis-atomic resonance fluorescence apparatus. The title reaction was studied under pseudo-first-order conditions in O atoms in an excess of ClO. ClO radicals were produced in the discharge flow tube by the reaction of Cl with either O3 or Cl2O and its concentration was measured in situ by UV absorption. O atoms were produced by pulsed laser photolysis of ClO at 308 nm and detected by atomic resonance fluorescence. The measurements yield k1(T) = (3.0 ± 0.8) × 10^-11 exp((75 ± 40)/T) cm³ molecule^-1 s^-1, where the uncertainties are at the 95% confidence level and include estimated systematic errors. These results are compared with previous data and an expression that can be used for atmospheric purposes is suggested.

To describe a variant of prion encephalopathy associated with the recently identified H187R mutation in the prion protein (PRNP) gene.

Hydrogen-bonded complexes of bromocyclopropane with the strong bases ammonia and trimethylamine have been isolated and characterized for the first time in argon matrices at 16 K. Coordination of the proton adjacent to the Br substituent on the cyclopropane ring to the nitrogen of the base was evidenced by distinct blue shifts of the C−H(Br) bending modes in the infrared spectrum. These shifts (~12 cm^-1 for the in-plane bend and ~6 cm^-1 for the out-of-plane bend) are much smaller than those observed for alkenes and alkynes, suggesting a distinct but extremely weak interaction. Ab initio calculations yield an essentially linear BrC−H···NH3 hydrogen bond with a C−H···N distance of 2.301 Å and a hydrogen bond energy of 2.35 kcal/mol, thus supporting that this hydrogen bond is one of the weakest observed thus far in a matrix. This study represents the first example of a (substituted) cyclopropane acting as a proton donor and only the second example of an alkane taking part in a C−H···N hydrogen bond.

The quantum yields for the production of Cl, O, and ClO in the photolysis of ClONO2, measured by detecting Cl and O atoms by atomic resonance fluorescence, are reported. The resonance fluorescence signals were calibrated by generating known concentrations of Cl and O atoms from the photolysis of Cl2, HCl, O3, or N2O. The quantum yields for Cl in the 193.2, 222.0, 248.25, and 308.15 nm photolysis of ClONO2 were 0.53 ± 0.10, 0.46 ± 0.10, 0.41 ± 0.13, and 0.64 ± 0.20, respectively. The yields for O atoms at these wavelengths were, respectively, 0.37 ± 0.08, 0.17 ± 0.05, <0.10, and <0.05. The quoted uncertainties are 2σ precision of the measurements. ClO radical was converted to Cl via addition of NO and its signal compared to the Cl atom signal produced by photolysis of ClONO2. The obtained quantum yields for ClO were 0.29 ± 0.20, 0.64 ± 0.20, 0.39 ± 0.19, and 0.37 ± 0.19, at 193.2, 222.0, 248.25, and 308.15 nm, respectively. It appears that Cl + NO3 and ClO + NO2 are the major products in the photodissociation of ClONO2, except at 193 nm. The measured quantum yields were found to be independent of pressure (40−100 Torr) and bath gas (He and N2). Our results are compared with those from previous measurements.

An American family of English origin with an unusually early onset and long-duration form of Creutzfeldt-Jakob disease (CJD) had a heterozygous insert mutation in the region of repeating octapeptide coding sequences between codons 51 and 91 of the PRNP gene on chromosome 20. Affected members were 23 to 35 years old at the onset of illnesses that lasted from 4 to 13 years, yet experimental transmission of disease from the proband (11-year duration) produced a typically brief incubation period and duration of illness in each of three inoculated primates. Also, the PrP amyloid protein that accumulates in CJD brain was only barely detectable in extracted brain tissue from one case with massive spongiform change and was undetectable in another case with no spongiform change, perhaps because of epitope shielding by a configurational change in the protein induced by the mutation. Analysis of this and other families with similar inserts suggests that such mutations in the PRNP gene not only predispose to CJD, but also modify its phenotypic expression.

The APOEgenotype has been shown to influence the risk of developing sporadic and familial AD. This effect is isoform-dependent, the APOE4 allele increasing susceptibility and the APOE2 allele providing protection. Amyloid formation is an important part of the pathogenesis in AD as well as in spongiform encephalopathies; apoE deposition in amyloid plaques has been documented in both conditions.

The rate coefficient for the reaction O(³P) with ClONO2, k1, was measured between 202 and 325 K using two methods:  pulsed laser photolysis with time-resolved atomic resonance fluorescence detection of the O atoms and pulsed laser photolysis with long-path tunable diode laser absorption for detection of NO3 radicals. The measured rate coefficient is summarized by k1 = (4.5 ± 1.4) × 10^-12 exp[(−900 ± 80)/T] cm³ molecule^-1 s^-1, with k1(298 K) = (2.2 ± 0.2) × 10^-13 cm³ molecule^-1 s^-1. The yield of NO3 radical in this reaction was measured to be essentially unity. Our results are compared with those from previous studies.

We report a family in which the proband died of clinically typical, neuropathologically verified Creutzfeldt-Jakob disease; her still-living mother suffers from a progressive dementia of many years' duration, and her maternal grandfather died after a similar illness. The proband, her mother, and two of three young first-degree relatives all have an identical insert mutation in the PRNPgene consisting of a twice-repeated 24-nucleotide sequence in the region between codons 51 and 91.

We tested DNA from 15 centrally infected cases of iatrogenic Creutzfeldt-Jakob disease (CJD) (dura mater or corneal homografts and stereotactic EEG electrodes), 11 peripherally infected cases (native human growth hormone or gonadotrophin), and 110 control individuals for the presence of mutations in the chromosome 20 amyloid gene. No patient or control had any of the known pathogenic point or insert mutations found in familial disease, but allelic homozygosity at polymorphic codon 129 was present in all but two (92) of the 26 patients, compared with 54 (50) of the 110 controls (p< 0.001). Pooled data from all identified and tested cases of iatrogenic disease yielded a worldwide total of 56 patients, of whom all but four were homozygous at codon 129 (p< 0.001). These findings support the thesis that homozygosity at codon 129 enhances susceptibility to iatrogenic infections of both central and peripheral origin, with evident implications for the population of dura mater homograft and pituitary hormone recipients whose lives have been complicated by the possibility of exposure to the infectious agent of CJD.