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&

Latest research on acute hepatopancreatic necrosis disease (AHPND) of penaeid shrimps

Acute hepatopancreatic necrosis disease (AHPND) is caused by unique strains of Vibrio parahaemolyticus (VPAHPND) and V. harveyi that have transferrable plasmid carrying the virulent PirAB-like toxin genes. The genomes of VPAHPND strains and V. harveyi from Thailand and Viet Nam, respectively, have been characterized by our group. The genome of VPAHPND strains from Mexico, Viet Nam, and China have also been studied by other groups. We have developed a conventional polymerase chain reaction (PCR) and loop-mediated isothermal amplification (LAMP) methods for the detection of AHPND using a primer set that targets the PirAB-like toxin genes of VPAHPND. We have characterized the toxin genes of VPAHPND strains and also constructed a recombinant plasmid (broad host range) carrying PirAB-like toxin genes. Non-VPAHPND strain N7 which does not carry the plasmid and strain FP11 which is carrying a plasmid not coding for the toxin genes were transformed with the plasmid carrying PirAB-like toxin genes. As a result, the transformed N7 and FP11 strains became virulent and killed whiteleg shrimp (Penaeus vannamei) similar to or at par with the virulence of VPAHPND strain. We then fed the whiteleg shrimp with commercial feed containing the formalin-killed VPAHPND strain. After 2 days of feeding, all of the whiteleg shrimp died. These results clearly indicate that the PirAB-like toxin is the virulence factor of VPAHPND. We have been investigating the virulence mechanism of the PirAB-like toxin produced by VPAHPND strains. First, we calculated the copy number of plasmid encoding the PirAB-like toxin genes of several VPAHPND strains. The copy number of the plasmid varied, ranging from 1 to 36 copies. Interestingly, VPAHPND strains carrying low copy number of plasmid were more virulent than VPAHPND strains carrying high copy number of the plasmid. These results imply that the copy number of toxin genes is not an important factor responsible for the degree of virulence of the VPAHPND strains. We are also studying other factors associated with the virulence of PirAB-like toxin. Likewise, we are developing prevention methods against AHPND including the use of formalin-killed cell vaccine, IgY additive in feed, and nano-bubble treatment of rearing water. This paper summarizes the current R&D on the disease

Complete Genome Sequences of Arcobacter butzleri ED-1 and Arcobacter sp Strain L, Both Isolated from a Microbial Fuel Cell

Arcobacter butzleri strain ED-1 is an exoelectrogenic epsilonproteobacterium isolated from the anode biofilm of a microbial fuel cell. Arcobacter sp. strain L dominates the liquid phase of the same fuel cell. Here we report the finished and annotated genome sequences of these organisms

Shrimp metabolism: The roles of lactate dehydrogenase (c31), glycogen phosphorylase (c34) and protein kinase (PK) as revealed by RNA interference

Abstract only.Energy metabolism is well-studied in vertebrate systems, providing insights on the genes and mechanisms involved in different pathways necessary for the survival of an organism. Yet, such studies are still lacking in invertebrate systems much more in shrimp. An earlier study has showed several contigs from the black tiger shrimp to be homologous to white spot syndrome virus (WSSV), a devastating pathogen in shrimp, including contig 31-WSSVORF82 (c31) and contig 34-WSSVORF21 (c34). This study aims to unveil the roles of three genes: c31, c34 and protein kinase (PK) in the shrimp system and its possible role in WSSV-infection. Rapid amplification of cDNA ends-polymerase chain reaction or RACE-PCR was used to obtain the full-length sequence of c31 and c34, followed by in vivo gene silencing using RNAi technology, and intramuscularly injecting dsRNA to WSSVchallenged Macrobrachium rosenbergii and Penaeus (Marsupenaeus) japonicus. Gene expression followed for healthy shrimps and dsRNA-treated shrimps. Mrc31 was revealed to be the enzyme lactase dehydrogenase (LDH), commonly released during tissue damage and is a marker for disease. The most parsimonious tree pictured Mrc31 to be sister clades to LDH of other shrimp species, Penaeus monodon and P. vannamei, supported with 100% and 72% bootstrap values, respectively. Mrc34 was highly homologous to the glycogen phosphorylase (GP) enzymes of other organisms including that of another shrimp, M. japonicus, bearing a bootstrap value of 99%. For PK, phylogenetic analysis revealed that the three open reading frames (ORFs) from P. monodon, M. rosenbergii and P. japonicus have 30% homology to WSSV-PK supported by a 98% bootstrap value. Mortality data from dsRNA-treated and WSSV-infected shrimps showed that treatment with dsRNA-LDH, GP and PK had significantly higher survival rates compared to that of the controls, Phosphate Buffered Saline (PBS) and Green Fluorescent Protein (GFP). Silencing the three genes in the shrimp has rendered some protective effect against the virus. Gene expression showed that all three genes are present in immune-related organs such as the gills, hepatopancreas and hemocyte. This study is the first to report the possible identities and functions of contigs 31, 34 and PK providing valuable data on the shrimp's genome