A star formation study of the ATLAS3D early-type galaxies with the AKARI all-sky survey

The star formation properties of early-type galaxies (ETGs) are currently the subject of considerable interest, particularly whether they differ from those of gas-rich spirals. We perform a systematic study of star formation in a large sample of local ETGs using polycyclic aromatic hydrocarbon (PAH) and dust emission, focusing on the galaxies' star formation rates (SFRs) and star formation efficiencies (SFEs). Our sample is composed of the 260 ETGs from the ATLAS3D survey, from which we use the cold gas measurements (HI and CO). The SFRs are estimated from stellar, PAH and dust fits to spectral energy distributions created from new AKARI measurements and literature data from WISE and 2MASS. The mid-infrared luminosities of non-CO-detected galaxies are well correlated with their stellar luminosities, showing that they trace (circum)stellar dust emission. CO-detected galaxies show an excess above these correlations, uncorrelated with their stellar luminosities, indicating that they likely contain PAHs and dust of interstellar origin. PAH and dust luminosities of CO-detected galaxies show tight correlations with their molecular gas masses, and the derived current SFRs are typically 0.01-1 Msun/yr. These SFRs systematically decrease with stellar age at fixed stellar mass, while they correlate nearly linearly with stellar mass at fixed age. The majority of local ETGs follow the same star-formation law as local star-forming galaxies, and their current SFEs do not depend on either stellar mass or age. Our results clearly indicate that molecular gas is fueling current star formation in local ETGs, that appear to acquire this gas via mechanisms regulated primarily by stellar mass. The current SFEs of local ETGs are similar to those of local star-forming galaxies, indicating that their low SFRs are likely due to smaller cold gas fractions rather than a suppression of star formation.Comment: 30 pages, 12 figures, 4 tables, accepted for publication in A&

Epigenetic inactivation of the NORE1 gene correlates with malignant progression of colorectal tumors

<p>Abstract</p> <p>Background</p> <p>NORE1 (RASSF5) is a newly described member of the RASSF family with Ras effector function. <it>NORE1 </it>expression is frequently inactivated by aberrant promoter hypermethylation in many human cancers, suggesting that NORE1 might be a putative tumor suppressor. However, expression and mutation status of <it>NORE1 </it>and its implication in colorectal tumorigenesis has not been evaluated.</p> <p>Methods</p> <p>Expression, mutation, and methylation status of <it>NORE1A </it>and <it>NORE1B </it>in 10 cancer cell lines and 80 primary tumors were characterized by quantitative PCR, SSCP, and bisulfite DNA sequencing analyses. Effect of NORE1A and NORE1B expression on tumor cell growth was evaluated using cell number counting, flow cytometry, and colony formation assays.</p> <p>Results</p> <p>Expression of <it>NORE1A </it>and <it>NORE1B </it>transcript was easily detectable in all normal colonic epithelial tissues, but substantially decreased in 7 (70%) and 4 (40%) of 10 cancer cell lines and 31 (38.8%) and 25 (31.3%) of 80 primary carcinoma tissues, respectively. Moreover, 46 (57.6%) and 38 (47.5%) of 80 matched tissue sets exhibited tumor-specific reduction of <it>NORE1A </it>and <it>NORE1B</it>, respectively. Abnormal reduction of <it>NORE1 </it>was more commonly observed in advanced stage and high grade tumors compared to early and low grade tumors. While somatic mutations of the gene were not identified, its expression was re-activated in all low expressor cells after treatment with the demethylating agent 5-aza-dC. Bisulfite DNA sequencing analysis of 31 CpG sites within the promoter region demonstrated that abnormal reduction of <it>NORE1A </it>is tightly associated with promoter CpG sites hypermethylation. Moreover, transient expression and siRNA-mediated knockdown assays revealed that both NORE1A and NORE1B decrease cellular growth and colony forming ability of tumor cells and enhance tumor cell response to apoptotic stress.</p> <p><b>Conclusion</b></p> <p>Our data indicate that epigenetic inactivation of <it>NORE1 </it>due to aberrant promoter hypermethylation is a frequent event in colorectal tumorigenesis and might be implicated in the malignant progression of colorectal tumors.</p

Aberrant DNA methylation associated with silencing BNIP3 gene expression in haematopoietic tumours

Hypoxia is a key factor contributing to the progression of human neoplasias and to the development of resistance to chemotherapy. BNIP3 is a proapoptotic member of the Bcl-2 protein family involved in hypoxia-induced cell death. We evaluated the expression and methylation status of BNIP3 gene to better understand the role of epigenetic alteration of its expression in haematopoietic tumours. Methylation of the region around the BNIP3 transcription start site was detected in four acute lymphocytic leukaemia, one multiple myeloma and one Burkitt lymphoma cell lines, and was closely associated with silencing the gene. That expression of BNIP3 was restored by treatment with 5-aza2′-deoxycytidine (5-aza-dC), a methyltransferase inhibitor, which confirmed the gene to be epigenetically inactivated by methylation. Notably, re-expression of BNIP3 using 5-aza2-dC also restored hypoxia-mediated cell death in methylated cell lines. Acetylation of histone H3 in the 5′ region of the gene, which was assessed using chromatin immunoprecipitation assays, correlated directly with gene expression and inversely with DNA methylation. Among primary tumours, methylation of BNIP3 was detected in five of 34 (15%) acute lymphocytic leukaemias, six of 35 (17%) acute myelogenous leukaemias and three of 14 (21%) multiple myelomas. These results suggest that aberrant DNA methylation of the 5′ CpG island and histone deacetylation play key roles in silencing BNIP3 expression in haematopoietic tumours

Epigenetic inactivation of TCF2 in ovarian cancer and various cancer cell lines

Transcription factor 2 gene (TCF2) encodes hepatocyte nuclear factor 1β (HNF1β), a transcription factor associated with development and metabolism. Mutation of TCF2 has been observed in renal cell cancer, and by screening aberrantly methylated genes, we have now identified TCF2 as a target for epigenetic inactivation in ovarian cancer. TCF2 was methylated in 53% of ovarian cancer cell lines and 26% of primary ovarian cancers, resulting in loss of the gene's expression. TCF2 expression was restored by treating cells with a methyltransferase inhibitor, 5-aza-2′deoxycitidine (5-aza-dC). In addition, chromatin immunoprecipitation showed deacetylation of histone H3 in methylated cells and, when combined with 5-aza-dC, the histone deacetylase inhibitor trichostatin A synergistically induced TCF2 expression. Epigenetic inactivation of TCF2 was also seen in colorectal, gastric and pancreatic cell lines, suggesting general involvement of epigenetic inactivation of TCF2 in tumorigenesis. Restoration of TCF2 expression induced expression of HNF4α, a transcriptional target of HNF1β, indicating that epigenetic silencing of TCF2 leads to alteration of the hepatocyte nuclear factor network in tumours. These results suggest that TCF2 is involved in the development of ovarian cancers and may represent a useful target for their detection and treatment

Characterization of nonpathogenic Cadophora gregata, a potential biological control agent, concomitantly isolated from soil infested with Cadophora gregata f. sp. adzukicola, the cause of adzuki bean brown stem rot

We collected 555 isolates of Cadophora gregata from adzuki bean field soils in Hokkaido, Japan, from 1997 to 2000. To identify the brown stem rot (BSR) pathogen C. gregata f. sp. adzukicola, we screened these isolates for pathogenicity to adzuki beans. Of the isolates, all of which originated in Tokachi District, Hokkaido, Japan, 23 were avirulent to adzuki bean, soybean, or mung bean. However, polymerase chain reaction (PCR) with specific primers for C. gregata f. sp. adzukicola (BSRA1 and BSRA2) detected the specific identifying DNA fragment in these isolates, and cluster analysis with inter-simple sequence repeat markers showed that the isolates were phylogenetically closer to strains that are virulent to adzuki bean. Thus, we concluded that the isolates were nonpathogenic C. gregata. A few selected isolates of the nonpathogenic C. gregata were effective at reducing BSR in vivo and show potential for development as biological control agents

Autumn potato seedling failure due to potato dry rot in Nagasaki Prefecture, Japan, caused by Fusarium acuminatum and Fusarium commune

Failure to sprout due to seed-tuber rot is a serious problem for autumn potato seedling cultivation in Nagasaki Prefecture, Japan. In this study, five strains were isolated from rotten seed tubers sampled in 2015; when tubers were inoculated with these strains, the tubers developed rot and failed to sprout. We identified these strains as Fusarium acuminatum, Fusarium commune, and the known agent of potato dry rot, Fusarium oxysporum based on morphological and DNA sequencing analyses. F. commune and F. acuminatum were identified as causal agents of potato dry for the first time in the world and in Japan, respectively

Soft rot of root chicory in Hokkaido and its causal bacteria

In August 2010, bacterial soft rot was found on root chicory (Cichorium intybus var. sativum) in Hokkaido, Japan. Severely infected plants in fields were discolored, had wilted foliage, and black necrosis of petioles near the crown. Wilted leaves subsequently collapsed and died, forming a dry, brown or black rosette. The root and crown became partially or wholly soft-rotted. Slimy masses on infected areas of roots, turned dark brown or black. Gram-negative, rod-shaped, peritrichously flagellated, facultatively anaerobic bacteria were exclusively isolated from rotted roots, and typical symptoms were reproduced after inoculation with the strains. The bacteria were identified as Dickeya dianthicola, Pectobacterium carotovorum subsp. carotovorum, and Pectobacterium carotovorum subsp. odoriferum based on further bacteriological characterization and the sequence analysis of the malate dehydrogenase gene and 16S rRNA gene. These bacteria should be included with the previously reported Dickeya (=Erwinia) chrysanthemi in Saitama Prefecture, Japan, as causal pathogens of bacterial wilt of chicory