ALBERT

Description: Vernalization, the acceleration of flowering by a long period of cold temperature, ensures that many plants overwinter vegetatively and flower in spring. In Arabidopsis, allelic variation at the FRIGIDA (FRI) locus is a major determinant of natural variation in flowering time. Dominant alleles of FRI confer late flowering, which is reversed to earliness by vernalization. We cloned FRI and analyzed the molecular basis of the allelic variation. Most of the early-flowering ecotypes analyzed carry FRI alleles containing one of two different deletions that disrupt the open reading frame. Loss-of-function mutations at FRI have thus provided the basis for the evolution of many early-flowering ecotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johanson, U -- West, J -- Lister, C -- Michaels, S -- Amasino, R -- Dean, C -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030654" target="_blank"〉PubMed〈/a〉

Description: Respondents in the 1988 General Social Survey (GSS) were asked to scan their acquaintance networks to identify all those who had been a victim of a homicide or had acquired immunodeficiency syndrome (AIDS). Estimates of the sex, race, age, and regional breakdowns for homicides in the last year and for people with AIDS were compared with official statistics. The GSS estimates for the distribution of homicide victims replicate the official statistics quite well. The GSS estimates for AIDS cases suggest that the data provided to the Centers for Disease Control may underestimate by a substantial margin the prevalence of AIDS in the white population of higher socioeconomic status, overstate the relative prevalence of the disease in the minority populations, underestimate the prevalence of the disease in the Midwest, and overstate it for the East.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laumann, E O -- Gagnon, J H -- Michaels, S -- Michael, R T -- Coleman, J S -- N0I-HD-8-2907/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1186-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Sociology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543079" target="_blank"〉PubMed〈/a〉

Description: Autism spectrum disorders (ASDs) are childhood neurodevelopmental disorders with complex genetic origins. Previous studies focusing on candidate genes or genomic regions have identified several copy number variations (CNVs) that are associated with an increased risk of ASDs. Here we present the results from a whole-genome CNV study on a cohort of 859 ASD cases and 1,409 healthy children of European ancestry who were genotyped with approximately 550,000 single nucleotide polymorphism markers, in an attempt to comprehensively identify CNVs conferring susceptibility to ASDs. Positive findings were evaluated in an independent cohort of 1,336 ASD cases and 1,110 controls of European ancestry. Besides previously reported ASD candidate genes, such as NRXN1 (ref. 10) and CNTN4 (refs 11, 12), several new susceptibility genes encoding neuronal cell-adhesion molecules, including NLGN1 and ASTN2, were enriched with CNVs in ASD cases compared to controls (P = 9.5 x 10(-3)). Furthermore, CNVs within or surrounding genes involved in the ubiquitin pathways, including UBE3A, PARK2, RFWD2 and FBXO40, were affected by CNVs not observed in controls (P = 3.3 x 10(-3)). We also identified duplications 55 kilobases upstream of complementary DNA AK123120 (P = 3.6 x 10(-6)). Although these variants may be individually rare, they target genes involved in neuronal cell-adhesion or ubiquitin degradation, indicating that these two important gene networks expressed within the central nervous system may contribute to the genetic susceptibility of ASD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925224/" 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/PMC2925224/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glessner, Joseph T -- Wang, Kai -- Cai, Guiqing -- Korvatska, Olena -- Kim, Cecilia E -- Wood, Shawn -- Zhang, Haitao -- Estes, Annette -- Brune, Camille W -- Bradfield, Jonathan P -- Imielinski, Marcin -- Frackelton, Edward C -- Reichert, Jennifer -- Crawford, Emily L -- Munson, Jeffrey -- Sleiman, Patrick M A -- Chiavacci, Rosetta -- Annaiah, Kiran -- Thomas, Kelly -- Hou, Cuiping -- Glaberson, Wendy -- Flory, James -- Otieno, Frederick -- Garris, Maria -- Soorya, Latha -- Klei, Lambertus -- Piven, Joseph -- Meyer, Kacie J -- Anagnostou, Evdokia -- Sakurai, Takeshi -- Game, Rachel M -- Rudd, Danielle S -- Zurawiecki, Danielle -- McDougle, Christopher J -- Davis, Lea K -- Miller, Judith -- Posey, David J -- Michaels, Shana -- Kolevzon, Alexander -- Silverman, Jeremy M -- Bernier, Raphael -- Levy, Susan E -- Schultz, Robert T -- Dawson, Geraldine -- Owley, Thomas -- McMahon, William M -- Wassink, Thomas H -- Sweeney, John A -- Nurnberger, John I -- Coon, Hilary -- Sutcliffe, James S -- Minshew, Nancy J -- Grant, Struan F A -- Bucan, Maja -- Cook, Edwin H -- Buxbaum, Joseph D -- Devlin, Bernie -- Schellenberg, Gerard D -- Hakonarson, Hakon -- 1U24MH081810/MH/NIMH NIH HHS/ -- HD055751/HD/NICHD NIH HHS/ -- HD055782-01/HD/NICHD NIH HHS/ -- HD35476/HD/NICHD NIH HHS/ -- M01 RR000064-340579/RR/NCRR NIH HHS/ -- M01 RR000064-350579/RR/NCRR NIH HHS/ -- M01 RR000064-35S10579/RR/NCRR NIH HHS/ -- M01 RR000064-35S10591/RR/NCRR NIH HHS/ -- M01 RR000064-35S10602/RR/NCRR NIH HHS/ -- M01 RR000064-35S20579/RR/NCRR NIH HHS/ -- M01 RR000064-35S20591/RR/NCRR NIH HHS/ -- M01 RR000064-35S20602/RR/NCRR NIH HHS/ -- M01 RR000064-360579/RR/NCRR NIH HHS/ -- M01 RR000064-360582/RR/NCRR NIH HHS/ -- M01 RR000064-360591/RR/NCRR NIH HHS/ -- M01 RR000064-36S10579/RR/NCRR NIH HHS/ -- M01 RR000064-36S10582/RR/NCRR NIH HHS/ -- M01 RR000064-36S10591/RR/NCRR NIH HHS/ -- M01 RR000064-370579/RR/NCRR NIH HHS/ -- M01 RR000064-370582/RR/NCRR NIH HHS/ -- M01 RR000064-370591/RR/NCRR NIH HHS/ -- M01 RR000064-37S10579/RR/NCRR NIH HHS/ -- M01 RR000064-37S10582/RR/NCRR NIH HHS/ -- M01 RR000064-37S10591/RR/NCRR NIH HHS/ -- M01 RR000064-380579/RR/NCRR NIH HHS/ -- M01 RR000064-380582/RR/NCRR NIH HHS/ -- M01 RR000064-380591/RR/NCRR NIH HHS/ -- M01 RR000064-390579/RR/NCRR NIH HHS/ -- M01 RR000064-390582/RR/NCRR NIH HHS/ -- M01 RR000064-390591/RR/NCRR NIH HHS/ -- M01-RR00064/RR/NCRR NIH HHS/ -- MH061009/MH/NIMH NIH HHS/ -- MH0666730/MH/NIMH NIH HHS/ -- MH64547/MH/NIMH NIH HHS/ -- MH69359/MH/NIMH NIH HHS/ -- NS049261/NS/NINDS NIH HHS/ -- P01 HD035476-03/HD/NICHD NIH HHS/ -- P01 HD035476-04/HD/NICHD NIH HHS/ -- P01 HD035476-04S1/HD/NICHD NIH HHS/ -- P01 HD035476-04S2/HD/NICHD NIH HHS/ -- P01 HD035476-05/HD/NICHD NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- P50 HD055751-01/HD/NICHD NIH HHS/ -- P50 HD055751-010002/HD/NICHD NIH HHS/ -- P50 HD055751-019003/HD/NICHD NIH HHS/ -- P50 HD055751-02/HD/NICHD NIH HHS/ -- P50 HD055751-020002/HD/NICHD NIH HHS/ -- P50 HD055751-03/HD/NICHD NIH HHS/ -- P50 HD055751-030002/HD/NICHD NIH HHS/ -- P50 HD055751-04/HD/NICHD NIH HHS/ -- P50 HD055782-01/HD/NICHD NIH HHS/ -- R01 MH057881/MH/NIMH NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH061009-01A1/MH/NIMH NIH HHS/ -- R01 MH061009-01A1S1/MH/NIMH NIH HHS/ -- R01 MH061009-02/MH/NIMH NIH HHS/ -- R01 MH061009-03/MH/NIMH NIH HHS/ -- R01 MH061009-04A1/MH/NIMH NIH HHS/ -- R01 MH061009-05/MH/NIMH NIH HHS/ -- R01 MH061009-06/MH/NIMH NIH HHS/ -- R01 MH061009-07/MH/NIMH NIH HHS/ -- R01 MH061009-08/MH/NIMH NIH HHS/ -- R01 MH064547/MH/NIMH NIH HHS/ -- R01 MH064547-01/MH/NIMH NIH HHS/ -- R01 MH064547-01S1/MH/NIMH NIH HHS/ -- R01 MH064547-02/MH/NIMH NIH HHS/ -- R01 MH064547-02S1/MH/NIMH NIH HHS/ -- R01 MH064547-03/MH/NIMH NIH HHS/ -- R01 MH064547-04/MH/NIMH NIH HHS/ -- R01 MH064547-05/MH/NIMH NIH HHS/ -- R01 MH069359/MH/NIMH NIH HHS/ -- R01 MH069359-01A2/MH/NIMH NIH HHS/ -- R01 MH069359-02/MH/NIMH NIH HHS/ -- R01 MH069359-03/MH/NIMH NIH HHS/ -- R01 MH069359-04/MH/NIMH NIH HHS/ -- R01 MH069359-05/MH/NIMH NIH HHS/ -- R01 NS049261/NS/NINDS NIH HHS/ -- R01 NS049261-01A2/NS/NINDS NIH HHS/ -- R01 NS049261-02/NS/NINDS NIH HHS/ -- R01 NS049261-03/NS/NINDS NIH HHS/ -- R01 NS049261-04/NS/NINDS NIH HHS/ -- R01 NS049261-05/NS/NINDS NIH HHS/ -- U10 MH066766-02S1/MH/NIMH NIH HHS/ -- U10MH66766-02S1/MH/NIMH NIH HHS/ -- U19 HD035476-06/HD/NICHD NIH HHS/ -- U19 HD035476-07/HD/NICHD NIH HHS/ -- U19 HD035476-08/HD/NICHD NIH HHS/ -- U19 HD035476-09/HD/NICHD NIH HHS/ -- U19 HD035476-10/HD/NICHD NIH HHS/ -- U24 MH081810/MH/NIMH NIH HHS/ -- U24 MH081810-01/MH/NIMH NIH HHS/ -- U24 MH081810-02/MH/NIMH NIH HHS/ -- U24 MH081810-03/MH/NIMH NIH HHS/ -- U24 MH081810-04/MH/NIMH NIH HHS/ -- U54 MH066673/MH/NIMH NIH HHS/ -- U54 MH066673-01A10001/MH/NIMH NIH HHS/ -- U54 MH066673-020001/MH/NIMH NIH HHS/ -- U54 MH066673-030001/MH/NIMH NIH HHS/ -- U54 MH066673-040001/MH/NIMH NIH HHS/ -- U54 MH066673-05/MH/NIMH NIH HHS/ -- U54 MH066673-050001/MH/NIMH NIH HHS/ -- UL1 RR024134/RR/NCRR NIH HHS/ -- UL1 RR024134-03/RR/NCRR NIH HHS/ -- UL1-RR024134-03/RR/NCRR NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2009 May 28;459(7246):569-73. doi: 10.1038/nature07953. Epub 2009 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19404257" target="_blank"〉PubMed〈/a〉

Description: In situ functional dissection of RNA cis -regulatory elements by multiplex CRISPR-Cas9 genome engineering In situ functional dissection of RNA 〈i〉cis〈/i〉-regulatory elements by multiplex CRISPR-Cas9 genome engineering, Published online: 13 December 2017; doi:10.1038/s41467-017-00686-2 RNA regulatory elements (RREs) are important post-transcriptional control features but studying them requires disrupting their activity without disturbing cellular homeostasis. Here the authors present GenERA, a CRISPR-Cas9 screening platform of in situ analysis of native RREs.