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  1. Artikel ; Online: Cholinergic systems are essential for late-stage maturation and refinement of motor cortical circuits.

    Ramanathan, Dhakshin S / Conner, James M / Anilkumar, Arjun A / Tuszynski, Mark H

    Journal of neurophysiology

    2015  Band 113, Heft 5, Seite(n) 1585–1597

    Abstract: Previous studies reported that early postnatal cholinergic lesions severely perturb early cortical development, impairing neuronal cortical migration and the formation of cortical dendrites and synapses. These severe effects of early postnatal ... ...

    Abstract Previous studies reported that early postnatal cholinergic lesions severely perturb early cortical development, impairing neuronal cortical migration and the formation of cortical dendrites and synapses. These severe effects of early postnatal cholinergic lesions preclude our ability to understand the contribution of cholinergic systems to the later-stage maturation of topographic cortical representations. To study cholinergic mechanisms contributing to the later maturation of motor cortical circuits, we first characterized the temporal course of cortical motor map development and maturation in rats. In this study, we focused our attention on the maturation of cortical motor representations after postnatal day 25 (PND 25), a time after neuronal migration has been accomplished and cortical volume has reached adult size. We found significant maturation of cortical motor representations after this time, including both an expansion of forelimb representations in motor cortex and a shift from proximal to distal forelimb representations to an extent unexplainable by simple volume enlargement of the neocortex. Specific cholinergic lesions placed at PND 24 impaired enlargement of distal forelimb representations in particular and markedly reduced the ability to learn skilled motor tasks as adults. These results identify a novel and essential role for cholinergic systems in the late refinement and maturation of cortical circuits. Dysfunctions in this system may constitute a mechanism of late-onset neurodevelopmental disorders such as Rett syndrome and schizophrenia.
    Mesh-Begriff(e) Animals ; Cholinergic Neurons/physiology ; Connectome ; Forelimb/innervation ; Male ; Motor Cortex/growth & development ; Motor Cortex/physiology ; Neurogenesis ; Psychomotor Performance ; Rats ; Rats, Inbred F344
    Sprache Englisch
    Erscheinungsdatum 2015-03-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80161-6
    ISSN 1522-1598 ; 0022-3077
    ISSN (online) 1522-1598
    ISSN 0022-3077
    DOI 10.1152/jn.00408.2014
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: TGF-β1-induced phospholamban expression alters esophageal smooth muscle cell contraction in patients with eosinophilic esophagitis.

    Beppu, Lisa Y / Anilkumar, Arjun A / Newbury, Robert O / Dohil, Ranjan / Broide, David H / Aceves, Seema S

    The Journal of allergy and clinical immunology

    2014  Band 134, Heft 5, Seite(n) 1100–1107.e4

    Abstract: Background: Eosinophilic esophagitis (EoE) is a chronic antigen-mediated disease characterized by esophageal eosinophilia, remodeling, and fibrosis. TGF-β1 is a central regulator of EoE remodeling and increases esophageal smooth muscle (ESM) cell ... ...

    Abstract Background: Eosinophilic esophagitis (EoE) is a chronic antigen-mediated disease characterized by esophageal eosinophilia, remodeling, and fibrosis. TGF-β1 is a central regulator of EoE remodeling and increases esophageal smooth muscle (ESM) cell contraction.
    Objective: In this study we aimed to understand the molecular mechanisms by which TGF-β1 could induce ESM cell contraction.
    Methods: We used primary human ESM cells and esophageal myofibroblasts (EMFs) to assess the mechanisms of TGF-β1-induced contraction. We analyzed the expression, phosphorylation, and function of phospholamban (PLN), a sarcoendoplasmic reticulum regulatory protein induced by TGF-β1. Expression of PLN, phospho-PLN, and its regulatory pathway was analyzed in the ESM of biopsy specimens from patients with EoE and control subjects. Gene silencing in EMFs from patients with EoE was used to understand the role of PLN in contraction.
    Results: TGF-β1 induced and phosphorylated PLN in primary human ESM cells and EMFs from patients with EoE. PLN and phospho-PLN levels were increased in smooth muscle from patients with EoE compared with that seen in smooth muscle from control subjects in vivo. PLN inhibition significantly diminished TGF-β1-induced EMF contraction in patients with EoE. PLN expression and ESM/EMF contraction depended on TGF-β receptor I signals.
    Conclusion: We describe a previously unrecognized mechanism for ESM cell contraction that depends on TGF-β1, its receptors, and PLN. Because PLN levels are increased in smooth muscle from patients with EoE and PLN silencing diminishes contraction, we provide a novel potential mechanistic framework and therapeutic target for ESM dysfunction in patients with EoE.
    Mesh-Begriff(e) Adult ; Calcium-Binding Proteins/biosynthesis ; Cells, Cultured ; Eosinophilic Esophagitis/metabolism ; Eosinophilic Esophagitis/pathology ; Eosinophilic Esophagitis/physiopathology ; Esophagus/metabolism ; Esophagus/pathology ; Esophagus/physiopathology ; Female ; Gene Expression Regulation ; Humans ; Male ; Muscle Contraction ; Muscle Proteins/metabolism ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Phosphorylation ; Transforming Growth Factor beta1/metabolism
    Chemische Substanzen Calcium-Binding Proteins ; Muscle Proteins ; TGFB1 protein, human ; Transforming Growth Factor beta1 ; phospholamban
    Sprache Englisch
    Erscheinungsdatum 2014-05-13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2014.04.004
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Anti-IL-5 therapy reduces mast cell and IL-9 cell numbers in pediatric patients with eosinophilic esophagitis.

    Otani, Iris M / Anilkumar, Arjun A / Newbury, Robert O / Bhagat, Monica / Beppu, Lisa Y / Dohil, Ranjan / Broide, David H / Aceves, Seema S

    The Journal of allergy and clinical immunology

    2013  Band 131, Heft 6, Seite(n) 1576–1582

    Abstract: Background: Eosinophilic esophagitis (EoE) is a clinicopathologic entity of increasing worldwide prevalence. IL-5 is essential for eosinophil trafficking, and anti-IL-5 therapy decreases esophageal eosinophilia. EoE is associated with prominent mast ... ...

    Abstract Background: Eosinophilic esophagitis (EoE) is a clinicopathologic entity of increasing worldwide prevalence. IL-5 is essential for eosinophil trafficking, and anti-IL-5 therapy decreases esophageal eosinophilia. EoE is associated with prominent mast cell infiltration.
    Objective: We investigated whether anti-IL-5 (mepolizumab) treatment reduced esophageal mast cell accumulation in biopsy specimens from pediatric patients with EoE from a previous randomized anti-IL-5 trial.
    Methods: A subanalysis was completed for children treated with 0.55, 2.5, or 10 mg/kg mepolizumab monthly for 12 weeks followed by no treatment until week 24. Quantitative immunochemistry was used to assess the numbers of eosinophils, tryptase-positive mast cells, IL-9(+) cells, and mast cell-eosinophil couplets before and after treatment.
    Results: Forty-three biopsy specimens had adequate tissue for paired analysis. Forty percent of subjects responded to anti-IL-5 (defined as <15 eosinophils per high-power field [hpf] after mepolizumab therapy), and 77% of all subjects had decreased numbers of mast cells after anti-IL-5. In responders epithelial mast cell numbers decreased from 62 to 19 per hpf (P < .001), were significantly lower than in nonresponders after therapy (P < .05), and correlated with eosinophil numbers (r = 0.75, P < .0001). Mast cells and eosinophils were found in couplets before therapy, and these were significantly decreased only in responders after anti-IL-5 (P < .001). Esophageal eosinophils comprised the majority of cells that made the mast cell growth factor IL-9. IL-9(+) cell numbers decreased from 102 to 71 per hpf (P < .001) after anti-IL-5.
    Conclusions: Pediatric patients with EoE had significantly fewer mast cells, IL-9(+) cells, and mast cell-eosinophil couplets in the esophageal epithelium after anti-IL-5 therapy. Because eosinophils were one source of IL-9, they might support esophageal mastocytosis.
    Mesh-Begriff(e) Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized/administration & dosage ; Antibodies, Monoclonal, Humanized/therapeutic use ; Cell Degranulation/drug effects ; Cell Degranulation/immunology ; Eosinophilia/immunology ; Eosinophilic Esophagitis/drug therapy ; Eosinophilic Esophagitis/immunology ; Eosinophilic Esophagitis/metabolism ; Esophagus/metabolism ; Humans ; Interleukin-5/antagonists & inhibitors ; Interleukin-9/metabolism ; Mast Cells/immunology ; Mucous Membrane/metabolism ; Tryptases/metabolism
    Chemische Substanzen Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Interleukin-5 ; Interleukin-9 ; mepolizumab (90Z2UF0E52) ; Tryptases (EC 3.4.21.59)
    Sprache Englisch
    Erscheinungsdatum 2013-04-25
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2013.02.042
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Anti–IL-5 therapy reduces mast cell and IL-9 cell numbers in pediatric patients with eosinophilic esophagitis

    Otani, Iris M / Anilkumar, Arjun A / Newbury, Robert O / Bhagat, Monica / Beppu, Lisa Y / Dohil, Ranjan / Broide, David H / Aceves, Seema S

    The Journal of Allergy and Clinical Immunology. 2013 June, v. 131, no. 6

    2013  

    Abstract: BACKGROUND: Eosinophilic esophagitis (EoE) is a clinicopathologic entity of increasing worldwide prevalence. IL-5 is essential for eosinophil trafficking, and anti–IL-5 therapy decreases esophageal eosinophilia. EoE is associated with prominent mast cell ...

    Abstract BACKGROUND: Eosinophilic esophagitis (EoE) is a clinicopathologic entity of increasing worldwide prevalence. IL-5 is essential for eosinophil trafficking, and anti–IL-5 therapy decreases esophageal eosinophilia. EoE is associated with prominent mast cell infiltration. OBJECTIVE: We investigated whether anti–IL-5 (mepolizumab) treatment reduced esophageal mast cell accumulation in biopsy specimens from pediatric patients with EoE from a previous randomized anti–IL-5 trial. METHODS: A subanalysis was completed for children treated with 0.55, 2.5, or 10 mg/kg mepolizumab monthly for 12 weeks followed by no treatment until week 24. Quantitative immunochemistry was used to assess the numbers of eosinophils, tryptase-positive mast cells, IL-9+ cells, and mast cell–eosinophil couplets before and after treatment. RESULTS: Forty-three biopsy specimens had adequate tissue for paired analysis. Forty percent of subjects responded to anti–IL-5 (defined as <15 eosinophils per high-power field [hpf] after mepolizumab therapy), and 77% of all subjects had decreased numbers of mast cells after anti–IL-5. In responders epithelial mast cell numbers decreased from 62 to 19 per hpf (P < .001), were significantly lower than in nonresponders after therapy (P < .05), and correlated with eosinophil numbers (r = 0.75, P < .0001). Mast cells and eosinophils were found in couplets before therapy, and these were significantly decreased only in responders after anti–IL-5 (P < .001). Esophageal eosinophils comprised the majority of cells that made the mast cell growth factor IL-9. IL-9+ cell numbers decreased from 102 to 71 per hpf (P < .001) after anti–IL-5. CONCLUSIONS: Pediatric patients with EoE had significantly fewer mast cells, IL-9+ cells, and mast cell–eosinophil couplets in the esophageal epithelium after anti–IL-5 therapy. Because eosinophils were one source of IL-9, they might support esophageal mastocytosis.
    Schlagwörter biopsy ; cell growth ; children ; eosinophilia ; eosinophils ; epithelium ; esophageal diseases ; immunochemistry ; interleukin-5 ; interleukin-9 ; mast cells ; patients
    Sprache Englisch
    Erscheinungsverlauf 2013-06
    Umfang p. 1576-1582.e2.
    Erscheinungsort Mosby, Inc.
    Dokumenttyp Artikel
    ZDB-ID 121011-7
    ISSN 1085-8725 ; 1097-6825 ; 0091-6749
    ISSN (online) 1085-8725 ; 1097-6825
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2013.02.042
    Datenquelle NAL Katalog (AGRICOLA)

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  5. Artikel ; Online: Drosophila muller f elements maintain a distinct set of genomic properties over 40 million years of evolution.

    Leung, Wilson / Shaffer, Christopher D / Reed, Laura K / Smith, Sheryl T / Barshop, William / Dirkes, William / Dothager, Matthew / Lee, Paul / Wong, Jeannette / Xiong, David / Yuan, Han / Bedard, James E J / Machone, Joshua F / Patterson, Seantay D / Price, Amber L / Turner, Bryce A / Robic, Srebrenka / Luippold, Erin K / McCartha, Shannon R /
    Walji, Tezin A / Walker, Chelsea A / Saville, Kenneth / Abrams, Marita K / Armstrong, Andrew R / Armstrong, William / Bailey, Robert J / Barberi, Chelsea R / Beck, Lauren R / Blaker, Amanda L / Blunden, Christopher E / Brand, Jordan P / Brock, Ethan J / Brooks, Dana W / Brown, Marie / Butzler, Sarah C / Clark, Eric M / Clark, Nicole B / Collins, Ashley A / Cotteleer, Rebecca J / Cullimore, Peterson R / Dawson, Seth G / Docking, Carter T / Dorsett, Sasha L / Dougherty, Grace A / Downey, Kaitlyn A / Drake, Andrew P / Earl, Erica K / Floyd, Trevor G / Forsyth, Joshua D / Foust, Jonathan D / Franchi, Spencer L / Geary, James F / Hanson, Cynthia K / Harding, Taylor S / Harris, Cameron B / Heckman, Jonathan M / Holderness, Heather L / Howey, Nicole A / Jacobs, Dontae A / Jewell, Elizabeth S / Kaisler, Maria / Karaska, Elizabeth A / Kehoe, James L / Koaches, Hannah C / Koehler, Jessica / Koenig, Dana / Kujawski, Alexander J / Kus, Jordan E / Lammers, Jennifer A / Leads, Rachel R / Leatherman, Emily C / Lippert, Rachel N / Messenger, Gregory S / Morrow, Adam T / Newcomb, Victoria / Plasman, Haley J / Potocny, Stephanie J / Powers, Michelle K / Reem, Rachel M / Rennhack, Jonathan P / Reynolds, Katherine R / Reynolds, Lyndsey A / Rhee, Dong K / Rivard, Allyson B / Ronk, Adam J / Rooney, Meghan B / Rubin, Lainey S / Salbert, Luke R / Saluja, Rasleen K / Schauder, Taylor / Schneiter, Allison R / Schulz, Robert W / Smith, Karl E / Spencer, Sarah / Swanson, Bryant R / Tache, Melissa A / Tewilliager, Ashley A / Tilot, Amanda K / VanEck, Eve / Villerot, Matthew M / Vylonis, Megan B / Watson, David T / Wurzler, Juliana A / Wysocki, Lauren M / Yalamanchili, Monica / Zaborowicz, Matthew A / Emerson, Julia A / Ortiz, Carlos / Deuschle, Frederic J / DiLorenzo, Lauren A / Goeller, Katie L / Macchi, Christopher R / Muller, Sarah E / Pasierb, Brittany D / Sable, Joseph E / Tucci, Jessica M / Tynon, Marykathryn / Dunbar, David A / Beken, Levent H / Conturso, Alaina C / Danner, Benjamin L / DeMichele, Gabriella A / Gonzales, Justin A / Hammond, Maureen S / Kelley, Colleen V / Kelly, Elisabeth A / Kulich, Danielle / Mageeney, Catherine M / McCabe, Nikie L / Newman, Alyssa M / Spaeder, Lindsay A / Tumminello, Richard A / Revie, Dennis / Benson, Jonathon M / Cristostomo, Michael C / DaSilva, Paolo A / Harker, Katherine S / Jarrell, Jenifer N / Jimenez, Luis A / Katz, Brandon M / Kennedy, William R / Kolibas, Kimberly S / LeBlanc, Mark T / Nguyen, Trung T / Nicolas, Daniel S / Patao, Melissa D / Patao, Shane M / Rupley, Bryan J / Sessions, Bridget J / Weaver, Jennifer A / Goodman, Anya L / Alvendia, Erica L / Baldassari, Shana M / Brown, Ashley S / Chase, Ian O / Chen, Maida / Chiang, Scott / Cromwell, Avery B / Custer, Ashley F / DiTommaso, Tia M / El-Adaimi, Jad / Goscinski, Nora C / Grove, Ryan A / Gutierrez, Nestor / Harnoto, Raechel S / Hedeen, Heather / Hong, Emily L / Hopkins, Barbara L / Huerta, Vilma F / Khoshabian, Colin / LaForge, Kristin M / Lee, Cassidy T / Lewis, Benjamin M / Lydon, Anniken M / Maniaci, Brian J / Mitchell, Ryan D / Morlock, Elaine V / Morris, William M / Naik, Priyanka / Olson, Nicole C / Osterloh, Jeannette M / Perez, Marcos A / Presley, Jonathan D / Randazzo, Matt J / Regan, Melanie K / Rossi, Franca G / Smith, Melanie A / Soliterman, Eugenia A / Sparks, Ciani J / Tran, Danny L / Wan, Tiffany / Welker, Anne A / Wong, Jeremy N / Sreenivasan, Aparna / Youngblom, Jim / Adams, Andrew / Alldredge, Justin / Bryant, Ashley / Carranza, David / Cifelli, Alyssa / Coulson, Kevin / Debow, Calise / Delacruz, Noelle / Emerson, Charlene / Farrar, Cassandra / Foret, Don / Garibay, Edgar / Gooch, John / Heslop, Michelle / Kaur, Sukhjit / Khan, Ambreen / Kim, Van / Lamb, Travis / Lindbeck, Peter / Lucas, Gabi / Macias, Elizabeth / Martiniuc, Daniela / Mayorga, Lissett / Medina, Joseph / Membreno, Nelson / Messiah, Shady / Neufeld, Lacey / Nguyen, San Francisco / Nichols, Zachary / Odisho, George / Peterson, Daymon / Rodela, Laura / Rodriguez, Priscilla / Rodriguez, Vanessa / Ruiz, Jorge / Sherrill, Will / Silva, Valeria / Sparks, Jeri / Statton, Geeta / Townsend, Ashley / Valdez, Isabel / Waters, Mary / Westphal, Kyle / Winkler, Stacey / Zumkehr, Joannee / DeJong, Randall J / Hoogewerf, Arlene J / Ackerman, Cheri M / Armistead, Isaac O / Baatenburg, Lara / Borr, Matthew J / Brouwer, Lindsay K / Burkhart, Brandon J / Bushhouse, Kelsey T / Cesko, Lejla / Choi, Tiffany Y Y / Cohen, Heather / Damsteegt, Amanda M / Darusz, Jess M / Dauphin, Cory M / Davis, Yelena P / Diekema, Emily J / Drewry, Melissa / Eisen, Michelle E M / Faber, Hayley M / Faber, Katherine J / Feenstra, Elizabeth / Felzer-Kim, Isabella T / Hammond, Brandy L / Hendriksma, Jesse / Herrold, Milton R / Hilbrands, Julia A / Howell, Emily J / Jelgerhuis, Sarah A / Jelsema, Timothy R / Johnson, Benjamin K / Jones, Kelly K / Kim, Anna / Kooienga, Ross D / Menyes, Erika E / Nollet, Eric A / Plescher, Brittany E / Rios, Lindsay / Rose, Jenny L / Schepers, Allison J / Scott, Geoff / Smith, Joshua R / Sterling, Allison M / Tenney, Jenna C / Uitvlugt, Chris / VanDyken, Rachel E / VanderVennen, Marielle / Vue, Samantha / Kokan, Nighat P / Agbley, Kwabea / Boham, Sampson K / Broomfield, Daniel / Chapman, Kayla / Dobbe, Ali / Dobbe, Ian / Harrington, William / Ibrahem, Marwan / Kennedy, Andre / Koplinsky, Chad A / Kubricky, Cassandra / Ladzekpo, Danielle / Pattison, Claire / Ramirez, Roman E / Wande, Lucia / Woehlke, Sarah / Wawersik, Matthew / Kiernan, Elizabeth / Thompson, Jeffrey S / Banker, Roxanne / Bartling, Justina R / Bhatiya, Chinmoy I / Boudoures, Anna L / Christiansen, Lena / Fosselman, Daniel S / French, Kristin M / Gill, Ishwar S / Havill, Jessen T / Johnson, Jaelyn L / Keny, Lauren J / Kerber, John M / Klett, Bethany M / Kufel, Christina N / May, Francis J / Mecoli, Jonathan P / Merry, Callie R / Meyer, Lauren R / Miller, Emily G / Mullen, Gregory J / Palozola, Katherine C / Pfeil, Jacob J / Thomas, Jessica G / Verbofsky, Evan M / Spana, Eric P / Agarwalla, Anant / Chapman, Julia / Chlebina, Ben / Chong, Insun / Falk, I N / Fitzgibbons, John D / Friedman, Harrison / Ighile, Osagie / Kim, Andrew J / Knouse, Kristin A / Kung, Faith / Mammo, Danny / Ng, Chun Leung / Nikam, Vinayak S / Norton, Diana / Pham, Philip / Polk, Jessica W / Prasad, Shreya / Rankin, Helen / Ratliff, Camille D / Scala, Victoria / Schwartz, Nicholas U / Shuen, Jessica A / Xu, Amy / Xu, Thomas Q / Zhang, Yi / Rosenwald, Anne G / Burg, Martin G / Adams, Stephanie J / Baker, Morgan / Botsford, Bobbi / Brinkley, Briana / Brown, Carter / Emiah, Shadie / Enoch, Erica / Gier, Chad / Greenwell, Alyson / Hoogenboom, Lindsay / Matthews, Jordan E / McDonald, Mitchell / Mercer, Amanda / Monsma, Nicholaus / Ostby, Kristine / Ramic, Alen / Shallman, Devon / Simon, Matthew / Spencer, Eric / Tomkins, Trisha / Wendland, Pete / Wylie, Anna / Wolyniak, Michael J / Robertson, Gregory M / Smith, Samuel I / DiAngelo, Justin R / Sassu, Eric D / Bhalla, Satish C / Sharif, Karim A / Choeying, Tenzin / Macias, Jason S / Sanusi, Fareed / Torchon, Karvyn / Bednarski, April E / Alvarez, Consuelo J / Davis, Kristen C / Dunham, Carrie A / Grantham, Alaina J / Hare, Amber N / Schottler, Jennifer / Scott, Zackary W / Kuleck, Gary A / Yu, Nicole S / Kaehler, Marian M / Jipp, Jacob / Overvoorde, Paul J / Shoop, Elizabeth / Cyrankowski, Olivia / Hoover, Betsy / Kusner, Matt / Lin, Devry / Martinov, Tijana / Misch, Jonathan / Salzman, Garrett / Schiedermayer, Holly / Snavely, Michael / Zarrasola, Stephanie / Parrish, Susan / Baker, Atlee / Beckett, Alissa / Belella, Carissa / Bryant, Julie / Conrad, Turner / Fearnow, Adam / Gomez, Carolina / Herbstsomer, Robert A / Hirsch, Sarah / Johnson, Christen / Jones, Melissa / Kabaso, Rita / Lemmon, Eric / Vieira, Carolina Marques Dos Santos / McFarland, Darryl / McLaughlin, Christopher / Morgan, Abbie / Musokotwane, Sepo / Neutzling, William / Nietmann, Jana / Paluskievicz, Christina / Penn, Jessica / Peoples, Emily / Pozmanter, Caitlin / Reed, Emily / Rigby, Nichole / Schmidt, Lasse / Shelton, Micah / Shuford, Rebecca / Tirasawasdichai, Tiara / Undem, Blair / Urick, Damian / Vondy, Kayla / Yarrington, Bryan / Eckdahl, Todd T / Poet, Jeffrey L / Allen, Alica B / Anderson, John E / Barnett, Jason M / Baumgardner, Jordan S / Brown, Adam D / Carney, Jordan E / Chavez, Ramiro A / Christgen, Shelbi L / Christie, Jordan S / Clary, Andrea N / Conn, Michel A / Cooper, Kristen M / Crowley, Matt J / Crowley, Samuel T / Doty, Jennifer S / Dow, Brian A / Edwards, Curtis R / Elder, Darcie D / Fanning, John P / Janssen, Bridget M / Lambright, Anthony K / Lane, Curtiss E / Limle, Austin B / Mazur, Tammy / McCracken, Marly R / McDonough, Alexa M / Melton, Amy D / Minnick, Phillip J / Musick, Adam E / Newhart, William H / Noynaert, Joseph W / Ogden, Bradley J / Sandusky, Michael W / Schmuecker, Samantha M / Shipman, Anna L / Smith, Anna L / Thomsen, Kristen M / Unzicker, Matthew R / Vernon, William B / Winn, Wesley W / Woyski, Dustin S / Zhu, Xiao / Du, Chunguang / Ament, Caitlin / Aso, Soham / Bisogno, Laura Simone / Caronna, Jason / Fefelova, Nadezhda / Lopez, Lenin / Malkowitz, Lorraine / Marra, Jonathan / Menillo, Daniella / Obiorah, Ifeanyi / Onsarigo, Eric Nyabeta / Primus, Shekerah / Soos, Mahdi / Tare, Archana / Zidan, Ameer / Jones, Christopher J / Aronhalt, Todd / Bellush, James M / Burke, Christa / DeFazio, Steve / Does, Benjamin R / Johnson, Todd D / Keysock, Nicholas / Knudsen, Nelson H / Messler, James / Myirski, Kevin / Rekai, Jade Lea / Rempe, Ryan Michael / Salgado, Michael S / Stagaard, Erica / Starcher, Justin R / Waggoner, Andrew W / Yemelyanova, Anastasia K / Hark, Amy T / Bertolet, Anne / Kuschner, Cyrus E / Parry, Kesley / Quach, Michael / Shantzer, Lindsey / Shaw, Mary E / Smith, Mary A / Glenn, Omolara / Mason, Portia / Williams, Charlotte / Key, S Catherine Silver / Henry, Tyneshia C P / Johnson, Ashlee G / White, Jackie X / Haberman, Adam / Asinof, Sam / Drumm, Kelly / Freeburg, Trip / Safa, Nadia / Schultz, Darrin / Shevin, Yakov / Svoronos, Petros / Vuong, Tam / Wellinghoff, Jules / Hoopes, Laura L M / Chau, Kim M / Ward, Alyssa / Regisford, E Gloria C / Augustine, LaJerald / Davis-Reyes, Brionna / Echendu, Vivienne / Hales, Jasmine / Ibarra, Sharon / Johnson, Lauriaun / Ovu, Steven / Braverman, John M / Bahr, Thomas J / Caesar, Nicole M / Campana, Christopher / Cassidy, Daniel W / Cognetti, Peter A / English, Johnathan D / Fadus, Matthew C / Fick, Cameron N / Freda, Philip J / Hennessy, Bryan M / Hockenberger, Kelsey / Jones, Jennifer K / King, Jessica E / Knob, Christopher R / Kraftmann, Karen J / Li, Linghui / Lupey, Lena N / Minniti, Carl J / Minton, Thomas F / Moran, Joseph V / Mudumbi, Krishna / Nordman, Elizabeth C / Puetz, William J / Robinson, Lauren M / Rose, Thomas J / Sweeney, Edward P / Timko, Ashley S / Paetkau, Don W / Eisler, Heather L / Aldrup, Megan E / Bodenberg, Jessica M / Cole, Mara G / Deranek, Kelly M / DeShetler, Megan / Dowd, Rose M / Eckardt, Alexandra K / Ehret, Sharon C / Fese, Jessica / Garrett, Amanda D / Kammrath, Anna / Kappes, Michelle L / Light, Morgan R / Meier, Anne C / O'Rouke, Allison / Perella, Mallory / Ramsey, Kimberley / Ramthun, Jennifer R / Reilly, Mary T / Robinett, Deirdre / Rossi, Nadine L / Schueler, Mary Grace / Shoemaker, Emma / Starkey, Kristin M / Vetor, Ashley / Vrable, Abby / Chandrasekaran, Vidya / Beck, Christopher / Hatfield, Kristen R / Herrick, Douglas A / Khoury, Christopher B / Lea, Charlotte / Louie, Christopher A / Lowell, Shannon M / Reynolds, Thomas J / Schibler, Jeanine / Scoma, Alexandra H / Smith-Gee, Maxwell T / Tuberty, Sarah / Smith, Christopher D / Lopilato, Jane E / Hauke, Jeanette / Roecklein-Canfield, Jennifer A / Corrielus, Maureen / Gilman, Hannah / Intriago, Stephanie / Maffa, Amanda / Rauf, Sabya A / Thistle, Katrina / Trieu, Melissa / Winters, Jenifer / Yang, Bib / Hauser, Charles R / Abusheikh, Tariq / Ashrawi, Yara / Benitez, Pedro / Boudreaux, Lauren R / Bourland, Megan / Chavez, Miranda / Cruz, Samantha / Elliott, GiNell / Farek, Jesse R / Flohr, Sarah / Flores, Amanda H / Friedrichs, Chelsey / Fusco, Zach / Goodwin, Zane / Helmreich, Eric / Kiley, John / Knepper, John Mark / Langner, Christine / Martinez, Megan / Mendoza, Carlos / Naik, Monal / Ochoa, Andrea / Ragland, Nicolas / Raimey, England / Rathore, Sunil / Reza, Evangelina / Sadovsky, Griffin / Seydoux, Marie-Isabelle B / Smith, Jonathan E / Unruh, Anna K / Velasquez, Vicente / Wolski, Matthew W / Gosser, Yuying / Govind, Shubha / Clarke-Medley, Nicole / Guadron, Leslie / Lau, Dawn / Lu, Alvin / Mazzeo, Cheryl / Meghdari, Mariam / Ng, Simon / Pamnani, Brad / Plante, Olivia / Shum, Yuki Kwan Wa / Song, Roy / Johnson, Diana E / Abdelnabi, Mai / Archambault, Alexi / Chamma, Norma / Gaur, Shailly / Hammett, Deborah / Kandahari, Adrese / Khayrullina, Guzal / Kumar, Sonali / Lawrence, Samantha / Madden, Nigel / Mandelbaum, Max / Milnthorp, Heather / Mohini, Shiv / Patel, Roshni / Peacock, Sarah J / Perling, Emily / Quintana, Amber / Rahimi, Michael / Ramirez, Kristen / Singhal, Rishi / Weeks, Corinne / Wong, Tiffany / Gillis, Aubree T / Moore, Zachary D / Savell, Christopher D / Watson, Reece / Mel, Stephanie F / Anilkumar, Arjun A / Bilinski, Paul / Castillo, Rostislav / Closser, Michael / Cruz, Nathalia M / Dai, Tiffany / Garbagnati, Giancarlo F / Horton, Lanor S / Kim, Dongyeon / Lau, Joyce H / Liu, James Z / Mach, Sandy D / Phan, Thu A / Ren, Yi / Stapleton, Kenneth E / Strelitz, Jean M / Sunjed, Ray / Stamm, Joyce / Anderson, Morgan C / Bonifield, Bethany Grace / Coomes, Daniel / Dillman, Adam / Durchholz, Elaine J / Fafara-Thompson, Antoinette E / Gross, Meleah J / Gygi, Amber M / Jackson, Lesley E / Johnson, Amy / Kocsisova, Zuzana / Manghelli, Joshua L / McNeil, Kylie / Murillo, Michael / Naylor, Kierstin L / Neely, Jessica / Ogawa, Emmy E / Rich, Ashley / Rogers, Anna / Spencer, J Devin / Stemler, Kristina M / Throm, Allison A / Van Camp, Matt / Weihbrecht, Katie / Wiles, T Aaron / Williams, Mallory A / Williams, Matthew / Zoll, Kyle / Bailey, Cheryl / Zhou, Leming / Balthaser, Darla M / Bashiri, Azita / Bower, Mindy E / Florian, Kayla A / Ghavam, Nazanin / Greiner-Sosanko, Elizabeth S / Karim, Helmet / Mullen, Victor W / Pelchen, Carly E / Yenerall, Paul M / Zhang, Jiayu / Rubin, Michael R / Arias-Mejias, Suzette M / Bermudez-Capo, Armando G / Bernal-Vega, Gabriela V / Colon-Vazquez, Mariela / Flores-Vazquez, Arelys / Gines-Rosario, Mariela / Llavona-Cartagena, Ivan G / Martinez-Rodriguez, Javier O / Ortiz-Fuentes, Lionel / Perez-Colomba, Eliezer O / Perez-Otero, Joseph / Rivera, Elisandra / Rodriguez-Giron, Luke J / Santiago-Sanabria, Arnaldo J / Senquiz-Gonzalez, Andrea M / delValle, Frank R Soto / Vargas-Franco, Dorianmarie / Velázquez-Soto, Karla I / Zambrana-Burgos, Joan D / Martinez-Cruzado, Juan Carlos / Asencio-Zayas, Lillyann / Babilonia-Figueroa, Kevin / Beauchamp-Pérez, Francis D / Belén-Rodríguez, Juliana / Bracero-Quiñones, Luciann / Burgos-Bula, Andrea P / Collado-Méndez, Xavier A / Colón-Cruz, Luis R / Correa-Muller, Ana I / Crooke-Rosado, Jonathan L / Cruz-García, José M / Defendini-Ávila, Marianna / Delgado-Peraza, Francheska M / Feliciano-Cancela, Alex J / Gónzalez-Pérez, Valerie M / Guiblet, Wilfried / Heredia-Negrón, Aldo / Hernández-Muñiz, Jennifer / Irizarry-González, Lourdes N / Laboy-Corales, Ángel L / Llaurador-Caraballo, Gabriela A / Marín-Maldonado, Frances / Marrero-Llerena, Ulises / Martell-Martínez, Héctor A / Martínez-Traverso, Idaliz M / Medina-Ortega, Kiara N / Méndez-Castellanos, Sonya G / Menéndez-Serrano, Krizia C / Morales-Caraballo, Carol I / Ortiz-DeChoudens, Saryleine / Ortiz-Ortiz, Patricia / Pagán-Torres, Hendrick / Pérez-Afanador, Diana / Quintana-Torres, Enid M / Ramírez-Aponte, Edwin G / Riascos-Cuero, Carolina / Rivera-Llovet, Michelle S / Rivera-Pagán, Ingrid T / Rivera-Vicéns, Ramón E / Robles-Juarbe, Fabiola / Rodríguez-Bonilla, Lorraine / Rodríguez-Echevarría, Brian O / Rodríguez-García, Priscila M / Rodríguez-Laboy, Abneris E / Rodríguez-Santiago, Susana / Rojas-Vargas, Michael L / Rubio-Marrero, Eva N / Santiago-Colón, Albeliz / Santiago-Ortiz, Jorge L / Santos-Ramos, Carlos E / Serrano-González, Joseline / Tamayo-Figueroa, Alina M / Tascón-Peñaranda, Edna P / Torres-Castillo, José L / Valentín-Feliciano, Nelson A / Valentín-Feliciano, Yashira M / Vargas-Barreto, Nadyan M / Vélez-Vázquez, Miguel / Vilanova-Vélez, Luis R / Zambrana-Echevarría, Cristina / MacKinnon, Christy / Chung, Hui-Min / Kay, Chris / Pinto, Anthony / Kopp, Olga R / Burkhardt, Joshua / Harward, Chris / Allen, Robert / Bhat, Pavan / Chang, Jimmy Hsiang-Chun / Chen, York / Chesley, Christopher / Cohn, Dara / DuPuis, David / Fasano, Michael / Fazzio, Nicholas / Gavinski, Katherine / Gebreyesus, Heran / Giarla, Thomas / Gostelow, Marcus / Greenstein, Rachel / Gunasinghe, Hashini / Hanson, Casey / Hay, Amanda / He, Tao Jian / Homa, Katie / Howe, Ruth / Howenstein, Jeff / Huang, Henry / Khatri, Aaditya / Kim, Young Lu / Knowles, Olivia / Kong, Sarah / Krock, Rebecca / Kroll, Matt / Kuhn, Julia / Kwong, Matthew / Lee, Brandon / Lee, Ryan / Levine, Kevin / Li, Yedda / Liu, Bo / Liu, Lucy / Liu, Max / Lousararian, Adam / Ma, Jimmy / Mallya, Allyson / Manchee, Charlie / Marcus, Joseph / McDaniel, Stephen / Miller, Michelle L / Molleston, Jerome M / Diez, Cristina Montero / Ng, Patrick / Ngai, Natalie / Nguyen, Hien / Nylander, Andrew / Pollack, Jason / Rastogi, Suchita / Reddy, Himabindu / Regenold, Nathaniel / Sarezky, Jon / Schultz, Michael / Shim, Jien / Skorupa, Tara / Smith, Kenneth / Spencer, Sarah J / Srikanth, Priya / Stancu, Gabriel / Stein, Andrew P / Strother, Marshall / Sudmeier, Lisa / Sun, Mengyang / Sundaram, Varun / Tazudeen, Noor / Tseng, Alan / Tzeng, Albert / Venkat, Rohit / Venkataram, Sandeep / Waldman, Leah / Wang, Tracy / Yang, Hao / Yu, Jack Y / Zheng, Yin / 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Chrystel / George, Eunice / Haltaufderhyde, Kirk / Haye, Joanna / Kaur, Manpreet / Semon, Max / Serjanov, Dmitri / Toorie, Anika / Wilson, Christopher / Riddle, Nicole C / Buhler, Jeremy / Mardis, Elaine R / Elgin, Sarah C R

    G3 (Bethesda, Md.)

    2015  Band 5, Heft 5, Seite(n) 719–740

    Abstract: The Muller F element (4.2 Mb, ~80 protein-coding genes) is an unusual autosome of Drosophila melanogaster; it is mostly heterochromatic with a low recombination rate. To investigate how these properties impact the evolution of repeats and genes, we ... ...

    Abstract The Muller F element (4.2 Mb, ~80 protein-coding genes) is an unusual autosome of Drosophila melanogaster; it is mostly heterochromatic with a low recombination rate. To investigate how these properties impact the evolution of repeats and genes, we manually improved the sequence and annotated the genes on the D. erecta, D. mojavensis, and D. grimshawi F elements and euchromatic domains from the Muller D element. We find that F elements have greater transposon density (25-50%) than euchromatic reference regions (3-11%). Among the F elements, D. grimshawi has the lowest transposon density (particularly DINE-1: 2% vs. 11-27%). F element genes have larger coding spans, more coding exons, larger introns, and lower codon bias. Comparison of the Effective Number of Codons with the Codon Adaptation Index shows that, in contrast to the other species, codon bias in D. grimshawi F element genes can be attributed primarily to selection instead of mutational biases, suggesting that density and types of transposons affect the degree of local heterochromatin formation. F element genes have lower estimated DNA melting temperatures than D element genes, potentially facilitating transcription through heterochromatin. Most F element genes (~90%) have remained on that element, but the F element has smaller syntenic blocks than genome averages (3.4-3.6 vs. 8.4-8.8 genes per block), indicating greater rates of inversion despite lower rates of recombination. Overall, the F element has maintained characteristics that are distinct from other autosomes in the Drosophila lineage, illuminating the constraints imposed by a heterochromatic milieu.
    Mesh-Begriff(e) Animals ; Codon ; Computational Biology ; DNA Transposable Elements ; Drosophila/genetics ; Drosophila Proteins/genetics ; Drosophila melanogaster/genetics ; Evolution, Molecular ; Exons ; Gene Rearrangement ; Genome ; Genomics ; Heterochromatin ; Introns ; Molecular Sequence Annotation ; Polytene Chromosomes ; Repetitive Sequences, Nucleic Acid ; Selection, Genetic ; Species Specificity
    Chemische Substanzen Codon ; DNA Transposable Elements ; Drosophila Proteins ; Heterochromatin
    Sprache Englisch
    Erscheinungsdatum 2015-03-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2629978-1
    ISSN 2160-1836 ; 2160-1836
    ISSN (online) 2160-1836
    ISSN 2160-1836
    DOI 10.1534/g3.114.015966
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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