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Articles by C Lin
Total Records ( 3 ) for C Lin
  M Mohan , H. M Herz , Y. H Takahashi , C Lin , K. C Lai , Y Zhang , M. P Washburn , L Florens and A. Shilatifard
 

Epigenetic modifications of chromatin play an important role in the regulation of gene expression. KMT4/Dot1 is a conserved histone methyltransferase capable of methylating chromatin on Lys79 of histone H3 (H3K79). Here we report the identification of a multisubunit Dot1 complex (DotCom), which includes several of the mixed lineage leukemia (MLL) partners in leukemia such as ENL, AF9/MLLT3, AF17/MLLT6, and AF10/MLLT10, as well as the known Wnt pathway modifiers TRRAP, Skp1, and β-catenin. We demonstrated that the human DotCom is indeed capable of trimethylating H3K79 and, given the association of β-catenin, Skp1, and TRRAP, we investigated, and found, a role for Dot1 in Wnt/Wingless signaling in an in vivo model system. Knockdown of Dot1 in Drosophila results in decreased expression of a subset of Wingless target genes. Furthermore, the loss of expression for the Drosophila homologs of the Dot1-associated proteins involved in the regulation of H3K79 shows a similar reduction in expression of these Wingless targets. From yeast to human, specific trimethylation of H3K79 by Dot1 requires the monoubiquitination of histone H2B by the Rad6/Bre1 complex. Here, we demonstrate that depletion of Bre1, the E3 ligase required for H2B monoubiquitination, leads specifically to reduced bulk H3K79 trimethylation levels and a reduction in expression of many Wingless targets. Overall, our study describes for the first time the components of DotCom and links the specific regulation of H3K79 trimethylation by Dot1 and its associated factors to the Wnt/Wingless signaling pathway.

  Temple The MGC Project Team , D. S Gerhard , R Rasooly , E. A Feingold , P. J Good , C Robinson , A Mandich , J. G Derge , J Lewis , D Shoaf , F. S Collins , W Jang , L Wagner , C. M Shenmen , L Misquitta , C. F Schaefer , K. H Buetow , T. I Bonner , L Yankie , M Ward , L Phan , A Astashyn , G Brown , C Farrell , J Hart , M Landrum , B. L Maidak , M Murphy , T Murphy , B Rajput , L Riddick , D Webb , J Weber , W Wu , K. D Pruitt , D Maglott , A Siepel , B Brejova , M Diekhans , R Harte , R Baertsch , J Kent , D Haussler , M Brent , L Langton , C. L.G Comstock , M Stevens , C Wei , M. J van Baren , K Salehi Ashtiani , R. R Murray , L Ghamsari , E Mello , C Lin , C Pennacchio , K Schreiber , N Shapiro , A Marsh , E Pardes , T Moore , A Lebeau , M Muratet , B Simmons , D Kloske , S Sieja , J Hudson , P Sethupathy , M Brownstein , N Bhat , J Lazar , H Jacob , C. E Gruber , M. R Smith , J McPherson , A. M Garcia , P. H Gunaratne , J Wu , D Muzny , R. A Gibbs , A. C Young , G. G Bouffard , R. W Blakesley , J Mullikin , E. D Green , M. C Dickson , A. C Rodriguez , J Grimwood , J Schmutz , R. M Myers , M Hirst , T Zeng , K Tse , M Moksa , M Deng , K Ma , D Mah , J Pang , G Taylor , E Chuah , A Deng , K Fichter , A Go , S Lee , J Wang , M Griffith , R Morin , R. A Moore , M Mayo , S Munro , S Wagner , S. J.M Jones , R. A Holt , M. A Marra , S Lu , S Yang , J Hartigan , M Graf , R Wagner , S Letovksy , J. C Pulido , K Robison , D Esposito , J Hartley , V. E Wall , R. F Hopkins , O Ohara and S. Wiemann
 

Since its start, the Mammalian Gene Collection (MGC) has sought to provide at least one full-protein-coding sequence cDNA clone for every human and mouse gene with a RefSeq transcript, and at least 6200 rat genes. The MGC cloning effort initially relied on random expressed sequence tag screening of cDNA libraries. Here, we summarize our recent progress using directed RT-PCR cloning and DNA synthesis. The MGC now contains clones with the entire protein-coding sequence for 92% of human and 89% of mouse genes with curated RefSeq (NM-accession) transcripts, and for 97% of human and 96% of mouse genes with curated RefSeq transcripts that have one or more PubMed publications, in addition to clones for more than 6300 rat genes. These high-quality MGC clones and their sequences are accessible without restriction to researchers worldwide.

  K Salehi Ashtiani , C Lin , T Hao , Y Shen , D Szeto , X Yang , L Ghamsari , H Lee , C Fan , R. R Murray , S Milstein , N Svrzikapa , M. E Cusick , F. P Roth , D. E Hill and M. Vidal
 

Although a highly accurate sequence of the Caenorhabditis elegans genome has been available for 10 years, the exact transcript structures of many of its protein-coding genes remain unsettled. Approximately two-thirds of the ORFeome has been verified reactively by amplifying and cloning computationally predicted transcript models; still a full third of the ORFeome remains experimentally unverified. To fully identify the protein-coding potential of the worm genome including transcripts that may not satisfy existing heuristics for gene prediction, we developed a computational and experimental platform adapting rapid amplification of cDNA ends (RACE) for large-scale structural transcript annotation. We interrogated 2000 unverified protein-coding genes using this platform. We obtained RACE data for approximately two-thirds of the examined transcripts and reconstructed ORF and transcript models for close to 1000 of these. We defined untranslated regions, identified new exons, and redefined previously annotated exons. Our results show that as much as 20% of the C. elegans genome may be incorrectly annotated. Many annotation errors could be corrected proactively with our large-scale RACE platform.

 
 
 
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