Regulation of phosphatidylinositol:ceramide phosphoinositol transferase in Saccharomyces cerevisiae.

Maximal phosphatidylinositol:ceramide phosphoinositol transferase activity was measured in yeast cells harvested during the exponential phase of growth. The addition of inositol to the growth medium resulted in a twofold increase in IPC synthase activity in cells grown in the presence or absence of exogenous choline. Enzyme activity was not regulated in yeast inositol biosynthesis regulatory mutants by the addition of inositol to the growth medium.     

Characterization of oil palm MADS box genes in relation to the mantled flower abnormality

In vitro propagation of oil palm (Elaeis guineensis Jacq.) frequently induces a somaclonal variant called ‘mantled’ abnormality, in which the stamens of both male and female flowers are transformed into carpels. This leads to a reduced yield or complete loss of the harvest of palm oil. The high frequency of the abnormality in independent lines and the high reversal rate suggest that it is due to an epigenetic change. The type of morphological changes suggest that it involves homeotic MADS box genes that regulate the identity of the flower whorls. We have isolated a number of MADS box genes from oil palm inflorescences by a MADS box-directed mRNA display approach. The isolated partial cDNAs included genes that were likely to function at the initial stages of flowering as well as genes that may function in determination of the inflorescence and the identity of the flower whorls. For four genes that were homologous to genes known to affect the reproductive parts of the flower, full length cDNAs were isolated. These were a B-type MADS box gene which may function in the determination of stamen formation, a C-type gene expected to be involved in stamen and carpel formation, and two putative SEP genes which act in concert with the A-, B- and C-type MADS box gene in determining flower whorl formation. The B-type gene EgMADS16 was functionally characterized as a PISTILLATA orthologue; it was able to complement an Arabidopsis thaliana pi mutant. Whether EgMADS16, or any of the other EgMADS genes, are functionally involved in the mantled condition remains to be established.     

Using spatially explicit commodity flow and truck activity data to map urban material flows

To analyze and promote resource efficiency in urban areas, it is important to characterize urban metabolism and particularly, material flows. Material flow analysis (MFA) offers a means to capture the dynamism of cities and their activities. Urban‐scale MFAs have been conducted in many cities, usually employing variants of the Eurostat methodology. However, current methodologies generally reduce the study area into a “black box,” masking details of the complex processes within the city's metabolism. Therefore, besides the aggregated stocks and flows of materials, the movement of materials—often embedded in goods or commodities—should also be highlighted. Understanding the movement and dispersion of goods and commodities can allow for more detailed analysis of material flows. We highlight the potential benefits of using high‐resolution urban commodity flows in the context of understanding material resource use and opportunities for conservation. Through the use of geographic information systems and visualizations, we analyze two spatially explicit datasets: (1) commodity flow data in the United States, and (2) Global Positioning System‐based commercial vehicle (truck) driver activity data in Singapore. In the age of “big data,” we bring advancements in freight data collection to the field of urban metabolism, uncovering the secondary sourcing of materials that would otherwise have been masked in typical MFA studies. This brings us closer to a consumption‐based, finer‐resolution approach to MFA, which more effectively captures human activities and its impact on urban environments.     

The AXB and BXA set of recombinant inbred mouse strains

The recombinant inbred (RI) set of strains, AXB and BXA, derived from C57BL/6J and A/J, originally constructed and maintained at the University of California/San Diego, have been imported into The Jackson Laboratory and are now in the 29th to 59th generation of brother-sister matings. Genetic quality control testing with 45 proviral and 11 biochemical markers previously typed in this RI set indicated that five strains had been genetically contaminated sometime in the past, so these strains have been discarded. The correct and complete strain distribution patterns for 56 genetic markers are reported for the remaining RI strain set, which consists of 31 living strains and 8 extinct strains for which DNA is available. Two additional strains, AXB 12 and BXA 17, are living and may be added to the set pending further tests of genetic purity. The progenitors of this RI set differ in susceptibility to 27 infectious diseases as well as atherosclerosis, obesity, diabetes, cancer, cleft palate, and hydrocephalus. Thus, the AXB and BXA set of RI strains will be useful in the genetic analysis of several complex diseases.     

Strain distribution pattern in AXB and BXA recombinant inbred strains for loci on murine Chromosomes 10, 13, 17, and 18

Strain distribution patterns (SDPs) of selected loci previously mapped to murine Chromosomes (Chrs) 10, 13, 17, and 18 are reported for the AXB, BXA recombinant inbred (RI) strain set derived from the progenitor strains A/J (A) and C57BL/6J (B). The loci included the simple sequence length polymorphisms (D10Nds1, D10Mit2, D10Mit10, D10Mit14, D13Mit3, D13Nds1, D13Mit10, D13Mit13, D13Mit7, D13Mit11, D17Mit18, D17Mit10, D17Mit20, D17Mit3, D17Mit2, D18Mit17, D18Mit9, and D18Mit4), the restriction fragment length polymorphisms Pdea and Csfmr, and the biochemical marker AS-1. These loci were chosen because they map to genomic regions that had few or no genetic markers in the AXB, BXA RI set. Several of these loci also were typed in backcross progeny of matings of the (AXB)F₁ to strain A or B. The strain distribution patterns for chromosomes 10, 13, 17, and 18 are reported, and the gene order and map distances determined from the backcross data. The addition of these markers to the AXB, BXA RI strain set increases the genomic region over which linkage for new markers can be detected.     

Genome-Wide Analysis of Copy Number Variation Identifies Candidate Gene Loci Associated with the Progression of Non-Alcoholic Fatty Liver Disease

Between 10 and 25% of individuals with non-alcoholic fatty liver disease (NAFLD) develop hepatic fibrosis leading to cirrhosis and hepatocellular carcinoma (HCC). To investigate the molecular basis of disease progression, we performed a genome-wide analysis of copy number variation (CNV) in a total of 49 patients with NAFLD [10 simple steatosis and 39 non-alcoholic steatohepatitis (NASH)] and 49 matched controls using high-density comparative genomic hybridization (CGH) microarrays. A total of 11 CNVs were found to be unique to individuals with simple steatosis, whilst 22 were common between simple steatosis and NASH, and 224 were unique to NASH. We postulated that these CNVs could be involved in the pathogenesis of NAFLD progression. After stringent filtering, we identified four rare and/or novel CNVs that may influence the pathogenesis of NASH. Two of these CNVs, located at 13q12.11 and 12q13.2 respectively, harbour the exportin 4 (XPO4) and phosphodiesterase 1B (PDE1B) genes which are already known to be involved in the etiology of liver cirrhosis and HCC. Cross-comparison of the genes located at these four CNV loci with genes already known to be associated with NAFLD yielded a set of genes associated with shared biological processes including cell death, the key process involved in ‘second hit’ hepatic injury. To our knowledge, this pilot study is the first to provide CNV information of potential relevance to the NAFLD spectrum. These data could prove invaluable in predicting patients at risk of developing NAFLD and more importantly, those who will subsequently progress to NASH.     

Genetic analysis of the rfb region of Shigella flexneri encoding the Y serotype O-antigen specificity

The gene cluster (rfb region) which determines the biosynthesis of the Shigella flexneri O-antigen of the Y serotype specificity was cloned from a S. flexneri serotype 2a strain. Two plasmids, pPM2212 and pPM2213, which conferred O-antigen biosynthesis were generated from separate cosmid clones by deletion with Clal. These plasmids expressed O-antigen in Escherichia coli K12 like that of the parental strain, as assessed by reactions to antisera in colony and Western immunoblots, sensitivity to bacteriophage Sf6, and by silver staining of lipopolysaccharides separated by sodium dodecyl sulphate/polyacrylamide gel electrophoresis. These plasmids also mediated O-antigen expression in an E. coli K12 rfb-delete background, indicating that all the necessary genes have been cloned. A detailed restriction map of the region has been constructed and analysis of various subclones has allowed the limits of the coding region for O-antigen biosynthesis to be defined to a maximum of 11 kb. Expression of these plasmids demonstrates a novel phenotype associated with control of lipopolysaccharide chain length. The gene(s) responsible maps adjacent to, but separate from, those associated with the biosynthesis of the O-antigen unit. Analysis of plasmid-encoded proteins in minicells and maxicells has facilitated the construction of a physical map. Finally, plasmid pPM-2212 was used to probe a collection of S. flexneri serotypes by Southern hybridization. With the exception of serotype 6, which appears to be unrelated, a similar pattern was found in all serotypes.