The Tully-Fisher relation for S0 galaxies

We present a study of the local B and K-band Tully-Fisher Relation (TFR) between absolute magnitude and maximum circular speed in S0 galaxies. To make this study, we have combined kinematic data, including a new high-quality spectral data set from the Fornax Cluster, with homogeneous photometry from the RC3 and 2MASS catalogues, to construct the largest sample of S0 galaxies ever used in a study of the TFR. Independent of environment, S0 galaxies are found to lie systematically below the TFR for nearby spirals in both optical and infrared bands. This offset can be crudely interpreted as arising from the luminosity evolution of spiral galaxies that have faded since ceasing star formation. However, we also find a large scatter in the TFR. We show that most of this scatter is intrinsic, not due to the observational uncertainties. The presence of such a large scatter means that the population of S0 galaxies cannot have formed exclusively by the above simple fading mechanism after all transforming at a single epoch. To better understand the complexity of the transformation mechanism, we have searched for correlations between the offset from the TFR and other properties of the galaxies such as their structural properties, central velocity dispersions and ages (as estimated from line indices). For the Fornax Cluster data, the offset from the TFR relates with the estimated age of the stars in the individual galaxies, in the sense and of the magnitude expected if S0 galaxies had passively faded since being converted from spirals. This correlation implies that a significant part of the scatter in the TFR arises from the different times at which galaxies began their transformation.Comment: 17 pages, 11 figures, 3 tables, accepted for publication in MNRA

Brief Report: The Deletion of the Phosphatase Regulator NIPP1 Causes Progenitor Cell Expansion in the Adult Liver

The Ppp1r8 gene encodes NIPP1, a nuclear interactor of protein phosphatase PP1. The deletion of NIPP1 is embryonic lethal at the gastrulation stage, which has hampered its functional characterization in adult tissues. Here, we describe the effects of a conditional deletion of NIPP1 in mouse liver epithelial cells. Ppp1r8(-/-) livers developed a ductular reaction, that is, bile-duct hyperplasia with associated fibrosis. The increased proliferation of biliary epithelial cells was at least partially due to an expansion of the progenitor cell compartment that was independent of liver injury. Gene-expression analysis confirmed an upregulation of progenitor cell markers in the liver knockout livers but showed no effect on the expression of liver-injury associated regulators of cholangiocyte differentiation markers. Consistent with an inhibitory effect of NIPP1 on progenitor cell proliferation, Ppp1r8(-/-) livers displayed an increased sensitivity to diet-supplemented 3,5-diethoxycarbonyl-1,4-dihydrocollidine, which also causes bile-duct hyperplasia through progenitor cell expansion. In contrast, the liver knockouts responded normally to injuries (partial hepatectomy, single CCl4 administration) that are restored through proliferation of differentiated parenchymal cells. Our data indicate that NIPP1 does not regulate the proliferation of hepatocytes but is a suppressor of biliary epithelial cell proliferation, including progenitor cells, in the adult liver. Stem Cells 2016;34:2256-2262.status: publishe

Molecular identification of the wheat male fertility gene Ms1 and its prospects for hybrid breeding

Heterosis can rapidly boost yield in crop species but development of hybrid-breeding systems for bread wheat remains a challenge. Here, Tucker et al. describe the molecular identification of the wheat Ms1 gene and discuss its potential for large-scale hybrid seed production in wheat