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  • Male  (14)
  • Spacecraft Design, Testing and Performance
  • Nature Publishing Group (NPG)  (14)
  • 1
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    Nature Publishing Group (NPG)
    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Virginia -- England -- Nature. 2010 Mar 18;464(7287):340-2. doi: 10.1038/464340a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237536" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antisocial Personality Disorder/physiopathology/psychology ; Child ; Female ; Forensic Sciences/ethics/*methods/trends ; Homicide/*legislation & jurisprudence/*psychology ; Humans ; Insanity Defense ; Magnetic Resonance Imaging/standards/*utilization ; Male ; *Neurosciences ; Positron-Emission Tomography/utilization ; Rape/legislation & jurisprudence/psychology ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-01-15
    Description: The human Y chromosome began to evolve from an autosome hundreds of millions of years ago, acquiring a sex-determining function and undergoing a series of inversions that suppressed crossing over with the X chromosome. Little is known about the recent evolution of the Y chromosome because only the human Y chromosome has been fully sequenced. Prevailing theories hold that Y chromosomes evolve by gene loss, the pace of which slows over time, eventually leading to a paucity of genes, and stasis. These theories have been buttressed by partial sequence data from newly emergent plant and animal Y chromosomes, but they have not been tested in older, highly evolved Y chromosomes such as that of humans. Here we finished sequencing of the male-specific region of the Y chromosome (MSY) in our closest living relative, the chimpanzee, achieving levels of accuracy and completion previously reached for the human MSY. By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content, indicating rapid evolution during the past 6 million years. The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor. We suggest that the extraordinary divergence of the chimpanzee and human MSYs was driven by four synergistic factors: the prominent role of the MSY in sperm production, 'genetic hitchhiking' effects in the absence of meiotic crossing over, frequent ectopic recombination within the MSY, and species differences in mating behaviour. Although genetic decay may be the principal dynamic in the evolution of newly emergent Y chromosomes, wholesale renovation is the paramount theme in the continuing evolution of chimpanzee, human and perhaps other older MSYs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653425/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653425/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Jennifer F -- Skaletsky, Helen -- Pyntikova, Tatyana -- Graves, Tina A -- van Daalen, Saskia K M -- Minx, Patrick J -- Fulton, Robert S -- McGrath, Sean D -- Locke, Devin P -- Friedman, Cynthia -- Trask, Barbara J -- Mardis, Elaine R -- Warren, Wesley C -- Repping, Sjoerd -- Rozen, Steve -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jan 28;463(7280):536-9. doi: 10.1038/nature08700. Epub 2010 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20072128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Y/*genetics ; DNA/chemistry/genetics ; Genes/*genetics ; Humans ; Male ; Molecular Sequence Data ; *Nucleic Acid Conformation ; Pan troglodytes/*genetics ; Sequence Homology, Nucleic Acid ; Y Chromosome/*genetics
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  • 3
    Publication Date: 2011-05-13
    Description: The acquired immunodeficiency syndrome (AIDS)-causing lentiviruses human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) effectively evade host immunity and, once established, infections with these viruses are only rarely controlled by immunological mechanisms. However, the initial establishment of infection in the first few days after mucosal exposure, before viral dissemination and massive replication, may be more vulnerable to immune control. Here we report that SIV vaccines that include rhesus cytomegalovirus (RhCMV) vectors establish indefinitely persistent, high-frequency, SIV-specific effector memory T-cell (T(EM)) responses at potential sites of SIV replication in rhesus macaques and stringently control highly pathogenic SIV(MAC239) infection early after mucosal challenge. Thirteen of twenty-four rhesus macaques receiving either RhCMV vectors alone or RhCMV vectors followed by adenovirus 5 (Ad5) vectors (versus 0 of 9 DNA/Ad5-vaccinated rhesus macaques) manifested early complete control of SIV (undetectable plasma virus), and in twelve of these thirteen animals we observed long-term (〉/=1 year) protection. This was characterized by: occasional blips of plasma viraemia that ultimately waned; predominantly undetectable cell-associated viral load in blood and lymph node mononuclear cells; no depletion of effector-site CD4(+) memory T cells; no induction or boosting of SIV Env-specific antibodies; and induction and then loss of T-cell responses to an SIV protein (Vif) not included in the RhCMV vectors. Protection correlated with the magnitude of the peak SIV-specific CD8(+) T-cell responses in the vaccine phase, and occurred without anamnestic T-cell responses. Remarkably, long-term RhCMV vector-associated SIV control was insensitive to either CD8(+) or CD4(+) lymphocyte depletion and, at necropsy, cell-associated SIV was only occasionally measurable at the limit of detection with ultrasensitive assays, observations that indicate the possibility of eventual viral clearance. Thus, persistent vectors such as CMV and their associated T(EM) responses might significantly contribute to an efficacious HIV/AIDS vaccine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102768/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102768/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, Scott G -- Ford, Julia C -- Lewis, Matthew S -- Ventura, Abigail B -- Hughes, Colette M -- Coyne-Johnson, Lia -- Whizin, Nathan -- Oswald, Kelli -- Shoemaker, Rebecca -- Swanson, Tonya -- Legasse, Alfred W -- Chiuchiolo, Maria J -- Parks, Christopher L -- Axthelm, Michael K -- Nelson, Jay A -- Jarvis, Michael A -- Piatak, Michael Jr -- Lifson, Jeffrey D -- Picker, Louis J -- HHSN261200800001E/PHS HHS/ -- HHSN272200900037C/PHS HHS/ -- P51 RR00163/RR/NCRR NIH HHS/ -- R01 AI060392/AI/NIAID NIH HHS/ -- R01 AI060392-05/AI/NIAID NIH HHS/ -- R24 RR016001/RR/NCRR NIH HHS/ -- R56 AI060392/AI/NIAID NIH HHS/ -- R56 AI060392-06/AI/NIAID NIH HHS/ -- U24 OD010850/OD/NIH HHS/ -- England -- Nature. 2011 May 26;473(7348):523-7. doi: 10.1038/nature10003. Epub 2011 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine and Gene Therapy Institute, Department of Molecular Microbiology, Oregon Health & Science University, Beaverton, Oregon 97006, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21562493" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Animals ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cytomegalovirus/genetics ; DNA, Viral/analysis ; Genetic Vectors/genetics ; Immunity, Mucosal/immunology ; Immunologic Memory/*immunology ; Macaca mulatta/blood/immunology/virology ; Male ; RNA, Viral/analysis ; SAIDS Vaccines/genetics/*immunology ; Simian Acquired Immunodeficiency Syndrome/blood/*immunology/*prevention & ; control/virology ; Simian Immunodeficiency Virus/growth & development/*immunology/isolation & ; purification/*pathogenicity ; T-Lymphocytes/*immunology ; Time Factors ; Vaccines, DNA/genetics/immunology ; Viral Load ; Virus Replication
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    Electronic ISSN: 1476-4687
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  • 4
    Publication Date: 2012-03-01
    Description: The human X and Y chromosomes evolved from an ordinary pair of autosomes during the past 200-300 million years. The human MSY (male-specific region of Y chromosome) retains only three percent of the ancestral autosomes' genes owing to genetic decay. This evolutionary decay was driven by a series of five 'stratification' events. Each event suppressed X-Y crossing over within a chromosome segment or 'stratum', incorporated that segment into the MSY and subjected its genes to the erosive forces that attend the absence of crossing over. The last of these events occurred 30 million years ago, 5 million years before the human and Old World monkey lineages diverged. Although speculation abounds regarding ongoing decay and looming extinction of the human Y chromosome, remarkably little is known about how many MSY genes were lost in the human lineage in the 25 million years that have followed its separation from the Old World monkey lineage. To investigate this question, we sequenced the MSY of the rhesus macaque, an Old World monkey, and compared it to the human MSY. We discovered that during the last 25 million years MSY gene loss in the human lineage was limited to the youngest stratum (stratum 5), which comprises three percent of the human MSY. In the older strata, which collectively comprise the bulk of the human MSY, gene loss evidently ceased more than 25 million years ago. Likewise, the rhesus MSY has not lost any older genes (from strata 1-4) during the past 25 million years, despite its major structural differences to the human MSY. The rhesus MSY is simpler, with few amplified gene families or palindromes that might enable intrachromosomal recombination and repair. We present an empirical reconstruction of human MSY evolution in which each stratum transitioned from rapid, exponential loss of ancestral genes to strict conservation through purifying selection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292678/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292678/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Jennifer F -- Skaletsky, Helen -- Brown, Laura G -- Pyntikova, Tatyana -- Graves, Tina -- Fulton, Robert S -- Dugan, Shannon -- Ding, Yan -- Buhay, Christian J -- Kremitzki, Colin -- Wang, Qiaoyan -- Shen, Hua -- Holder, Michael -- Villasana, Donna -- Nazareth, Lynne V -- Cree, Andrew -- Courtney, Laura -- Veizer, Joelle -- Kotkiewicz, Holland -- Cho, Ting-Jan -- Koutseva, Natalia -- Rozen, Steve -- Muzny, Donna M -- Warren, Wesley C -- Gibbs, Richard A -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- R01 HG000257-17/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 22;483(7387):82-6. doi: 10.1038/nature10843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. jhughes@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22367542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Y/*genetics ; Conserved Sequence/*genetics ; Crossing Over, Genetic/genetics ; *Evolution, Molecular ; Gene Amplification/genetics ; *Gene Deletion ; Humans ; In Situ Hybridization, Fluorescence ; Macaca mulatta/*genetics ; Male ; Models, Genetic ; Molecular Sequence Data ; Pan troglodytes/genetics ; Radiation Hybrid Mapping ; Selection, Genetic/genetics ; Time Factors ; Y Chromosome/*genetics
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  • 5
    Publication Date: 2013-09-13
    Description: Established infections with the human and simian immunodeficiency viruses (HIV and SIV, respectively) are thought to be permanent with even the most effective immune responses and antiretroviral therapies only able to control, but not clear, these infections. Whether the residual virus that maintains these infections is vulnerable to clearance is a question of central importance to the future management of millions of HIV-infected individuals. We recently reported that approximately 50% of rhesus macaques (RM; Macaca mulatta) vaccinated with SIV protein-expressing rhesus cytomegalovirus (RhCMV/SIV) vectors manifest durable, aviraemic control of infection with the highly pathogenic strain SIVmac239 (ref. 5). Here we show that regardless of the route of challenge, RhCMV/SIV vector-elicited immune responses control SIVmac239 after demonstrable lymphatic and haematogenous viral dissemination, and that replication-competent SIV persists in several sites for weeks to months. Over time, however, protected RM lost signs of SIV infection, showing a consistent lack of measurable plasma- or tissue-associated virus using ultrasensitive assays, and a loss of T-cell reactivity to SIV determinants not in the vaccine. Extensive ultrasensitive quantitative PCR and quantitative PCR with reverse transcription analyses of tissues from RhCMV/SIV vector-protected RM necropsied 69-172 weeks after challenge did not detect SIV RNA or DNA sequences above background levels, and replication-competent SIV was not detected in these RM by extensive co-culture analysis of tissues or by adoptive transfer of 60 million haematolymphoid cells to naive RM. These data provide compelling evidence for progressive clearance of a pathogenic lentiviral infection, and suggest that some lentiviral reservoirs may be susceptible to the continuous effector memory T-cell-mediated immune surveillance elicited and maintained by cytomegalovirus vectors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3849456/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3849456/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, Scott G -- Piatak, Michael Jr -- Ventura, Abigail B -- Hughes, Colette M -- Gilbride, Roxanne M -- Ford, Julia C -- Oswald, Kelli -- Shoemaker, Rebecca -- Li, Yuan -- Lewis, Matthew S -- Gilliam, Awbrey N -- Xu, Guangwu -- Whizin, Nathan -- Burwitz, Benjamin J -- Planer, Shannon L -- Turner, John M -- Legasse, Alfred W -- Axthelm, Michael K -- Nelson, Jay A -- Fruh, Klaus -- Sacha, Jonah B -- Estes, Jacob D -- Keele, Brandon F -- Edlefsen, Paul T -- Lifson, Jeffrey D -- Picker, Louis J -- HHSN261200800001E/PHS HHS/ -- P01 AI094417/AI/NIAID NIH HHS/ -- P51OD011092/OD/NIH HHS/ -- R01 AI060392/AI/NIAID NIH HHS/ -- R01 DE021291/DE/NIDCR NIH HHS/ -- R37 AI054292/AI/NIAID NIH HHS/ -- U19 AI095985/AI/NIAID NIH HHS/ -- U19 AI096109/AI/NIAID NIH HHS/ -- U24 OD010850/OD/NIH HHS/ -- U42 OD010426/OD/NIH HHS/ -- England -- Nature. 2013 Oct 3;502(7469):100-4. doi: 10.1038/nature12519. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine and Gene Therapy Institute and Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97006, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025770" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytomegalovirus/genetics/immunology ; Female ; Macaca mulatta ; Male ; Molecular Sequence Data ; SAIDS Vaccines/*immunology ; Simian Acquired Immunodeficiency Syndrome/*prevention & control/virology ; Simian Immunodeficiency Virus/*immunology ; Time Factors ; Vaccines, Attenuated/immunology ; Viral Load ; Virus Replication/physiology
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  • 6
    Publication Date: 2013-11-01
    Description: To understand the processes that maintain genetic diversity is a long-standing challenge in evolutionary biology, with implications for predicting disease resistance, response to environmental change, and population persistence. Simple population genetic models are not sufficient to explain the high levels of genetic diversity sometimes observed in ecologically important traits. In guppies (Poecilia reticulata), male colour pattern is both diverse and heritable, and is arguably one of the most extreme examples of morphological polymorphism known. Negative frequency-dependent selection (NFDS), a form of selection in which genotypes are favoured when they are rare, can potentially maintain such extensive polymorphism, but few experimental studies have confirmed its operation in nature. Here we use highly replicated experimental manipulations of natural populations to show that males with rare colour patterns have higher reproductive fitness, demonstrating NFDS mediated by sexual selection. Rare males acquired more mates and sired more offspring compared to common males and, as previously reported, had higher rates of survival. Orange colour, implicated in other studies of sexual selection in guppies, did predict male reproductive success, but only in one of three populations. These data support the hypothesis that NFDS maintains diversity in the colour patterns of male guppies through two selective agents, mates and predators. Similar field-based manipulations of genotype frequencies could provide a powerful approach to reveal the underlying ecological and behavioural mechanisms that maintain genetic and phenotypic diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Kimberly A -- Houde, Anne E -- Price, Anna C -- Rodd, F Helen -- England -- Nature. 2013 Nov 7;503(7474):108-10. doi: 10.1038/nature12717. Epub 2013 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science, 319 Stadium Drive, Florida State University, Tallahassee, Florida 32306, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24172904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Wild/genetics/*physiology ; Female ; Fertility/genetics/physiology ; Genetic Fitness/genetics/*physiology ; Genetic Variation/genetics ; Male ; Mating Preference, Animal/*physiology ; Models, Animal ; Phenotype ; Pigmentation/genetics/physiology ; Poecilia/genetics/*physiology ; Predatory Behavior ; Rivers ; Selection, Genetic/genetics/physiology ; Survival Rate
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  • 7
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    Nature Publishing Group (NPG)
    Publication Date: 2014-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Virginia -- England -- Nature. 2014 Apr 17;508(7496):296-7. doi: 10.1038/508296a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24740043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbohydrate Metabolism/genetics ; Depression/genetics ; Epigenesis, Genetic/genetics ; Female ; Heredity/*genetics ; Hippocampus/metabolism ; Humans ; Male ; Mice ; MicroRNAs/*analysis/blood/*genetics ; Models, Genetic ; Parent-Child Relations ; Receptors, Glucocorticoid/metabolism ; Spermatozoa/*metabolism ; Stress, Psychological/*genetics
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-03-25
    Description: Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. The paper by Nowak et al. has the evolution of eusociality as its title, but it is mostly about something else. It argues against inclusive fitness theory and offers an alternative modelling approach that is claimed to be more fundamental and general, but which, we believe, has no practical biological meaning for the evolution of eusociality. Nowak et al. overlook the robust empirical observation that eusociality has only arisen in clades where mothers are associated with their full-sibling offspring; that is, in families where the average relatedness of offspring to siblings is as high as to their own offspring, independent of population structure or ploidy. We believe that this omission makes the paper largely irrelevant for understanding the evolution of eusociality.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boomsma, Jacobus J -- Beekman, Madeleine -- Cornwallis, Charlie K -- Griffin, Ashleigh S -- Holman, Luke -- Hughes, William O H -- Keller, Laurent -- Oldroyd, Benjamin P -- Ratnieks, Francis L W -- England -- Nature. 2011 Mar 24;471(7339):E4-5; author reply E9-10. doi: 10.1038/nature09832.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430722" target="_blank"〉PubMed〈/a〉
    Keywords: *Altruism ; Animals ; *Biological Evolution ; Cooperative Behavior ; Female ; Game Theory ; Genetic Fitness ; Genetics, Population ; Male ; *Models, Biological ; Reproducibility of Results ; Reproduction/physiology ; Selection, Genetic ; Sex Ratio ; *Siblings
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  • 9
    Publication Date: 2014-02-28
    Description: Commitment to and completion of sexual development are essential for malaria parasites (protists of the genus Plasmodium) to be transmitted through mosquitoes. The molecular mechanism(s) responsible for commitment have been hitherto unknown. Here we show that PbAP2-G, a conserved member of the apicomplexan AP2 (ApiAP2) family of DNA-binding proteins, is essential for the commitment of asexually replicating forms to sexual development in Plasmodium berghei, a malaria parasite of rodents. PbAP2-G was identified from mutations in its encoding gene, PBANKA_143750, which account for the loss of sexual development frequently observed in parasites transmitted artificially by blood passage. Systematic gene deletion of conserved ApiAP2 genes in Plasmodium confirmed the role of PbAP2-G and revealed a second ApiAP2 member (PBANKA_103430, here termed PbAP2-G2) that significantly modulates but does not abolish gametocytogenesis, indicating that a cascade of ApiAP2 proteins are involved in commitment to the production and maturation of gametocytes. The data suggest a mechanism of commitment to gametocytogenesis in Plasmodium consistent with a positive feedback loop involving PbAP2-G that could be exploited to prevent the transmission of this pernicious parasite.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105895/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105895/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, Abhinav -- Hughes, Katie R -- Modrzynska, Katarzyna K -- Otto, Thomas D -- Pfander, Claudia -- Dickens, Nicholas J -- Religa, Agnieszka A -- Bushell, Ellen -- Graham, Anne L -- Cameron, Rachael -- Kafsack, Bjorn F C -- Williams, April E -- Llinas, Manuel -- Berriman, Matthew -- Billker, Oliver -- Waters, Andrew P -- 083811/Wellcome Trust/United Kingdom -- 083811/Z/07/Z/Wellcome Trust/United Kingdom -- 085349/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 104111/Wellcome Trust/United Kingdom -- G0501670/Medical Research Council/United Kingdom -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50GM071508/GM/NIGMS NIH HHS/ -- R01 AI076276/AI/NIAID NIH HHS/ -- T32 GM007388/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Mar 13;507(7491):253-7. doi: 10.1038/nature12970. Epub 2014 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Wellcome Trust Centre for Molecular Parasitology, University of Glasgow, Glasgow G12 8QQ, UK [2]. ; 1] Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK [2]. ; Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; Wellcome Trust Centre for Molecular Parasitology, University of Glasgow, Glasgow G12 8QQ, UK. ; Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA. ; 1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA [2] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA. ; 1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA [2] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA [3] Department of Biochemistry and Molecular Biology and Center for Infectious Disease Dynamics, The Pennsylvania State University, State College, Pennsylvania 16802, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/parasitology ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Feedback, Physiological ; Female ; Gene Expression Regulation ; Germ Cells/cytology/*growth & development/metabolism ; Malaria/*parasitology ; Male ; Mutation/genetics ; Plasmodium berghei/cytology/*genetics/*physiology ; Protein Transport ; Protozoan Proteins/genetics/*metabolism ; Reproduction, Asexual ; Sexual Development/*genetics ; Transcription, Genetic
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  • 10
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    Nature Publishing Group (NPG)
    Publication Date: 2014-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Virginia -- England -- Nature. 2014 Mar 6;507(7490):22-4. doi: 10.1038/507022a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24598623" target="_blank"〉PubMed〈/a〉
    Keywords: Acetophenones/pharmacology ; Animals ; Cellular Reprogramming/genetics ; Conditioning, Classical ; DNA Methylation/genetics ; Environmental Exposure ; Epigenesis, Genetic/drug effects/*genetics ; *Fathers ; Female ; Gene Silencing ; Genome, Human/genetics ; Genomic Imprinting ; Heredity/*genetics ; Histones/chemistry/metabolism ; Humans ; Male ; Mice ; MicroRNAs/genetics/metabolism ; *Models, Genetic ; Odors/analysis ; Plants/genetics/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; Protamines/metabolism ; Receptors, Odorant/genetics/metabolism ; Semen/chemistry/metabolism ; Spermatozoa/*metabolism ; Uncertainty
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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