Chemical Abundances of Seven Irregular and Three Tidal Dwarf Galaxies in the M81 Group

We have derived nebular abundances for 10 dwarf galaxies belonging to the M81 Group, including several galaxies which do not have abundances previously reported in the literature. For each galaxy, multiple H \ii regions were observed with GMOS-N at the Gemini Observatory in order to determine abundances of several elements (oxygen, nitrogen, sulfur, neon, and argon). For seven galaxies, at least one H \ii region had a detection of the temperature sensitive [OIII] $\lambda$4363 line, allowing a "direct" determination of the oxygen abundance. No abundance gradients were detected in the targeted galaxies and the observed oxygen abundances are typically in agreement with the well known metallicity-luminosity relation. However, three candidate "tidal dwarf" galaxies lie well off this relation, UGC 5336, Garland, and KDG 61. The nature of these systems suggests that UGC 5336 and Garland are indeed recently formed systems, whereas KDG 61 is most likely a dwarf spheroidal galaxy which lies along the same line of sight as the M81 tidal debris field. We propose that these H \ii regions formed from previously enriched gas which was stripped from nearby massive galaxies (e.g., NGC 3077 and M81) during a recent tidal interaction.Comment: 37 pages, 10 figures, accepted for publication in ApJ. Slit positions in Table 2 have been update

Antlia Dwarf Galaxy: Distance, quantitative morphology and recent formation history via statistical field correction

We apply a statistical field correction technique originally designed to determine membership of high redshift galaxy clusters to Hubble Space Telescope imaging of the Antlia Dwarf Galaxy; a galaxy at the very edge of the Local Group. Using the tip of the red giant branch standard candle method coupled with a simple Sobel edge detection filter we find a new distance to Antlia of 1.31 +/- 0.03 Mpc. For the first time for a Local Group Member, we compute the concentration, asymmetry and clumpiness (CAS) quantitative morphology parameters for Antlia from the distribution of resolved stars in the HST/ACS field, corrected with a new method for contaminants and complement these parameters with the Gini coefficient (G) and the second order moment of the brightest 20 per cent of the flux (M_20). We show that it is a classic dwarf elliptical (C = 2.0, A = 0.063, S = 0.077, G = 0.39 and M_20 = -1.17 in the F814W band), but has an appreciable blue stellar population at its core, confirming on-going star-formation. The values of asymmetry and clumpiness, as well as Gini and M_20 are consistent with an undisturbed galaxy. Although our analysis suggests that Antlia may not be tidally influenced by NGC 3109 it does not necessarily preclude such interaction.Comment: Accepted for publication in MNRA

Lilliput

Catalog for the exhibition Lilliput held at the Seton Hall University Walsh Gallery, June 8 - July 24, 2009. Curated by Jeanne Brasile and Asha Ganpat. Includes an essay by Jeanne Brasile and Asha Ganpat. Includes color illustrations

3D genomics across the tree of life reveals condensin II as a determinant of architecture type

We investigated genome folding across the eukaryotic tree of life. We find two types of three-dimensional(3D) genome architectures at the chromosome scale. Each type appears and disappears repeatedlyduring eukaryotic evolution. The type of genome architecture that an organism exhibits correlates with theabsence of condensin II subunits. Moreover, condensin II depletion converts the architecture of thehuman genome to a state resembling that seen in organisms such as fungi or mosquitoes. In this state,centromeres cluster together at nucleoli, and heterochromatin domains merge. We propose a physicalmodel in which lengthwise compaction of chromosomes by condensin II during mitosis determineschromosome-scale genome architecture, with effects that are retained during the subsequent interphase.This mechanism likely has been conserved since the last common ancestor of all eukaryotes.C.H. is supported by the Boehringer Ingelheim Fonds; C.H., Á.S.C., and B.D.R. are supported by an ERC CoG (772471, “CohesinLooping”); A.M.O.E. and B.D.R. are supported by the Dutch Research Council (NWO-Echo); and J.A.R. and R.H.M. are supported by the Dutch Cancer Society (KWF). T.v.S. and B.v.S. are supported by NIH Common Fund “4D Nucleome” Program grant U54DK107965. H.T. and E.d.W. are supported by an ERC StG (637597, “HAP-PHEN”). J.A.R., T.v.S., H.T., R.H.M., B.v.S., and E.d.W. are part of the Oncode Institute, which is partly financed by the Dutch Cancer Society. Work at the Center for Theoretical Biological Physics is sponsored by the NSF (grants PHY-2019745 and CHE-1614101) and by the Welch Foundation (grant C-1792). V.G.C. is funded by FAPESP (São Paulo State Research Foundation and Higher Education Personnel) grants 2016/13998-8 and 2017/09662-7. J.N.O. is a CPRIT Scholar in Cancer Research. E.L.A. was supported by an NSF Physics Frontiers Center Award (PHY-2019745), the Welch Foundation (Q-1866), a USDA Agriculture and Food Research Initiative grant (2017-05741), the Behavioral Plasticity Research Institute (NSF DBI-2021795), and an NIH Encyclopedia of DNA Elements Mapping Center Award (UM1HG009375). Hi-C data for the 24 species were created by the DNA Zoo Consortium (www.dnazoo.org). DNA Zoo is supported by Illumina, Inc.; IBM; and the Pawsey Supercomputing Center. P.K. is supported by the University of Western Australia. L.L.M. was supported by NIH (1R01NS114491) and NSF awards (1557923, 1548121, and 1645219) and the Human Frontiers Science Program (RGP0060/2017). The draft A. californica project was supported by NHGRI. J.L.G.-S. received funding from the ERC (grant agreement no. 740041), the Spanish Ministerio de Economía y Competitividad (grant no. BFU2016-74961-P), and the institutional grant Unidad de Excelencia María de Maeztu (MDM-2016-0687). R.D.K. is supported by NIH grant RO1DK121366. V.H. is supported by NIH grant NIH1P41HD071837. K.M. is supported by a MEXT grant (20H05936). M.C.W. is supported by the NIH grants R01AG045183, R01AT009050, R01AG062257, and DP1DK113644 and by the Welch Foundation. E.F. was supported by NHGR

Iron Uptake via DMT1 Integrates Cell Cycle with JAK-STAT3 Signaling to Promote Colorectal Tumorigenesis

Dietary iron intake and systemic iron balance are implicated in colorectal cancer (CRC) development, but the means by which iron contributes to CRC are unclear. Gene expression and functional studies demonstrated that the cellular iron importer, divalent metal transporter 1 (DMT1), is highly expressed in CRC through hypoxia-inducible factor 2alpha-dependent transcription. Colon-specific Dmt1 disruption resulted in a tumor-selective inhibitory effect of proliferation in mouse colon tumor models. Proteomic and genomic analyses identified an iron-regulated signaling axis mediated by cyclin-dependent kinase 1 (CDK1), JAK1, and STAT3 in CRC progression. A pharmacological inhibitor of DMT1 antagonized the ability of iron to promote tumor growth in a CRC mouse model and a patient-derived CRC enteroid orthotopic model. Our studies implicate a growth-promoting signaling network instigated by elevated intracellular iron levels in tumorigenesis, offering molecular insights into how a key dietary component may contribute to CRC