scholarly journals Evolution of the RNA N6-Methyladenosine Methylome Mediated by Genomic Duplication

2019 ◽  
Vol 182 (1) ◽  
pp. 345-360 ◽  
Author(s):  
Zhenyan Miao ◽  
Ting Zhang ◽  
Yuhong Qi ◽  
Jie Song ◽  
Zhaoxue Han ◽  
...  
Keyword(s):  
Genomic Duplication

scholarly journals A Genomic Duplication is Associated with Ectopic Eomesodermin Expression in the Embryonic Chicken Comb and Two Duplex-comb Phenotypes

PLoS Genetics ◽  
2015 ◽  
Vol 11 (3) ◽  
pp. e1004947 ◽  
Author(s):  
Ben Dorshorst ◽  
Mohammad Harun-Or-Rashid ◽  
Alireza Jian Bagherpoor ◽  
Carl-Johan Rubin ◽  
Chris Ashwell ◽  
...  
Keyword(s):  
Embryonic Chicken ◽  
Genomic Duplication

scholarly journals Genomic duplication problems for unrooted gene trees

BMC Genomics ◽  
2016 ◽  
Vol 17 (S1) ◽  
Author(s):  
Jarosław Paszek ◽  
Paweł Górecki
Keyword(s):  
Gene Trees ◽  
Genomic Duplication

scholarly journals A Novel Gene Amplification Causes Upregulation of the PatAB ABC Transporter and Fluoroquinolone Resistance in Streptococcus pneumoniae

2015 ◽  
Vol 59 (6) ◽  
pp. 3098-3108 ◽  
Author(s):  
Alison J. Baylay ◽  
Alasdair Ivens ◽  
Laura J. V. Piddock
Keyword(s):  
Antibiotic Resistance ◽  
Streptococcus Pneumoniae ◽  
Abc Transporter ◽  
Stress Responses ◽  
Fluorescent Protein ◽  
Gene Dosage ◽  
Fluoroquinolone Resistance ◽  
Reporter System ◽  
Content Type ◽  
Genomic Duplication

ABSTRACTOverexpression of the ABC transporter genespatAandpatBconfers efflux-mediated fluoroquinolone resistance inStreptococcus pneumoniaeand is also linked to pneumococcal stress responses. Although upregulation ofpatABhas been observed in many laboratory mutants and clinical isolates, the regulatory mechanisms controlling expression of these genes are unknown. In this study, we aimed to identify the cause of high-level constitutive overexpression ofpatABin M184, a multidrug-resistant mutant of S.pneumoniaeR6. Using a whole-genome transformation and sequencing approach, we identified a novel duplication of a 9.2-kb region of the M184 genome which included thepatABgenes. This duplication did not affect growth and was semistable with a low segregation rate. The expression levels ofpatABin M184 were much higher than those that could be fully explained by doubling of the gene dosage alone, and inactivation of the first copy ofpatAhad no effect on multidrug resistance. Using a green fluorescent protein reporter system, increasedpatABexpression was ascribed to transcriptional read-through from a tRNA gene upstream of the second copy ofpatAB. This is the first report of a large genomic duplication causing antibiotic resistance inS. pneumoniaeand also of a genomic duplication causing antibiotic resistance by a promoter switching mechanism.

A 4.6 kb genomic duplication on 20p12.2-12.3 is associated with brachydactyly type A2 in a Chinese family

2011 ◽  
Vol 48 (5) ◽  
pp. 312-316 ◽  
Author(s):  
P. Su ◽  
H. Ding ◽  
D. Huang ◽  
Y. Zhou ◽  
W. Huang ◽  
...  
Keyword(s):  
Chinese Family ◽  
Genomic Duplication

scholarly journals Intron gain by tandem genomic duplication: a novel case and a new version of the model

2016 ◽  
Author(s):  
Ming-Yue Ma ◽  
Xin-Ran Lan ◽  
Deng-Ke Niu
Keyword(s):  
Intron Gain ◽  
Spliceosomal Introns ◽  
Branch Site ◽  
Eukaryotic Gene ◽  
Exonic Splicing Enhancers ◽  
Exonic Sequence ◽  
Exon Structure ◽  
Splicing Site ◽  
Genomic Duplication ◽  
Gc Contents

Origin and subsequent accumulation of spliceosomal introns are prominent events in the evolution of eukaryotic gene structure. Recently gained introns would be especially useful for the study of the mechanisms of intron gain because randomly accumulated mutations might erase the evolutionary traces. The mechanisms of intron gain remain unclear due to the presence of very few solid cases. A widely cited model of intron gain is tandem genomic duplication, in which the duplication of an AGGT-containing exonic segment provides the GT and AG splicing sites for the new intron. We found that the second intron of the potato RNA-dependent RNA polymerase gene PGSC0003DMG402000361 originated mainly from a direct duplication of the 3′ side of the upstream intron. The 5' splicing site of this new intron was recruited from the upstream exonic sequence. In addition to the new intron, a downstream exonic segment of 178 bp also arose from duplication. Most of the splicing signals were inherited directly from the parental intron/exon structure, including a putative branch site, the polypyrimidine tract, the 3′ splicing site, two putative exonic splicing enhancers and the GC contents differentiated between the intron and exon. We propose a new version of the tandem genomic duplication model, termed as the partial duplication of the preexisting intron/exon structure. This new version and the widely cited version are not mutually exclusive.

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