scholarly journals Lineage-Specific Gene Duplication and Loss in Human and Great Ape Evolution

PLoS Biology ◽  
2004 ◽  
Vol 2 (7) ◽  
pp. e207 ◽  
Author(s):  
Andrew Fortna ◽  
Young Kim ◽  
Erik MacLaren ◽  
Kriste Marshall ◽  
Gretchen Hahn ◽  
...  
Keyword(s):  
Gene Duplication ◽  
Specific Gene ◽  
Great Ape ◽  
Gene Duplication And Loss ◽  
Ape Evolution ◽  
Lineage Specific Gene

scholarly journals Papain-like cysteine proteases in Carica papaya: lineage-specific gene duplication and expansion

BMC Genomics ◽  
2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Juan Liu ◽  
Anupma Sharma ◽  
Marie Jamille Niewiara ◽  
Ratnesh Singh ◽  
Ray Ming ◽  
...  
Keyword(s):  
Gene Duplication ◽  
Carica Papaya ◽  
Cysteine Proteases ◽  
Specific Gene ◽  
Lineage Specific Gene

scholarly journals Rapid Rates of Lineage-Specific Gene Duplication and Deletion in the α-Globin Gene Family

2008 ◽  
Vol 25 (3) ◽  
pp. 591-602 ◽  
Author(s):  
Federico G. Hoffmann ◽  
Juan C. Opazo ◽  
Jay F. Storz
Keyword(s):  
Gene Duplication ◽  
Gene Family ◽  
Globin Gene ◽  
Specific Gene ◽  
Lineage Specific Gene

scholarly journals Lineage-Specific Gene Expansions in Bacterial and Archaeal Genomes

2001 ◽  
Vol 11 (4) ◽  
pp. 555-565 ◽  
Author(s):  
I. King Jordan ◽  
Kira S. Makarova ◽  
John L. Spouge ◽  
Yuri I. Wolf ◽  
Eugene V. Koonin
Keyword(s):  
Gene Duplication ◽  
Average Score ◽  
Specific Gene ◽  
Tandem Gene Duplication ◽  
New Genes ◽  
A Genome ◽  
Prokaryotic Genomes ◽  
Bacterial Chromosomes ◽  
Large Clusters ◽  
Lineage Specific Gene

Gene duplication is an important mechanistic antecedent to the evolution of new genes and novel biochemical functions. In an attempt to assess the contribution of gene duplication to genome evolution in archaea and bacteria, clusters of related genes that appear to have expanded subsequent to the diversification of the major prokaryotic lineages (lineage-specific expansions) were analyzed. Analysis of 21 completely sequenced prokaryotic genomes shows that lineage-specific expansions comprise a substantial fraction (∼5%–33%) of their coding capacities. A positive correlation exists between the fraction of the genes taken up by lineage-specific expansions and the total number of genes in a genome. Consistent with the notion that lineage-specific expansions are made up of relatively recently duplicated genes, >90% of the detected clusters consists of only two to four genes. The more common smaller clusters tend to include genes with higher pairwise similarity (as reflected by average score density) than larger clusters. Regardless of size, cluster members tend to be located more closely on bacterial chromosomes than expected by chance, which could reflect a history of tandem gene duplication. In addition to the small clusters, almost all genomes also contain rare large clusters of size ≥20. Several examples of the potential adaptive significance of these large clusters are explored. The presence or absence of clusters and their related genes was used as the basis for the construction of a similarity graph for completely sequenced prokaryotic genomes. The topology of the resulting graph seems to reflect a combined effect of common ancestry, horizontal transfer, and lineage-specific gene loss.

scholarly journals Deep Evaluation to the Evolution History of Heat Shock Factor (HSF) Gene Family and Its Expansion Pattern in Seed Plants

2020 ◽  
Author(s):  
Yiying Liao ◽  
Zhiming Liu ◽  
Andrew W. Gichira ◽  
Min Yang ◽  
Ruth Wambui Mbichi ◽  
...  
Keyword(s):  
Heat Shock ◽  
Gene Duplication ◽  
Gene Family ◽  
Phylogenetic Reconstruction ◽  
Heat Shock Factor ◽  
Specific Gene ◽  
Ancestral State ◽  
Duplication Events ◽  
History Of ◽  
Lineage Specific Gene

Abstract BackgroundHSF (Heat shock factor) genes are essential in the irreplaceable functions in some of the basic developmental pathways in plants. Despite the extensive studies on the structure, function diversification, and evolution of HSF, their divergent history and gene duplication pattern remain unsolved. To further illustrate the probable divergent patterns in these subfamilies, we visited the evolutionary history of the HSF via phylogenetic reconstruction and genomic syntenic analyses by taking advantage of the increased sampling of genomic data for pteridophyta, gymnosperms and basal angiosperms. ResultsWe identified a novel clade including HSFA2, HSFA6, HSFA7, HSFA9 with complex relationship, very likely due to orthologous or paralogous genes retained after frequent gene duplication events. We suggested that HSFA9 was derived from HSFA2 through gene duplication in eudicots at ancestral state, and then expanded in a lineage-specific way. Our findings indicated that HSFB3 and HSFB5 emerged before the divergence of ancestral angiosperms, but were lost in common ancestors of monocots. We also presumed that HSFC2 was derived from HSFC1 in ancestral monocots. ConclusionThis work proposes that in the era of early differentiation of angiosperms during the radiation of flowering plants, the member size of HSF gene family was also being adjusted, accompanied with considerable sub- or neo-functionalization. The independent evolution of HSFs in eudicots and monocots, including lineage-specific gene duplication gave rise to a new gene in ancestral eudicots and monocots, and lineage-specific gene loss in ancestral monocots. Our analyses provide essential insights for studying evolution history of multigene family.

ISDN2012_0241: Developmental and evolutionary functions of a human‐specific gene duplication of srGAP2 during brain development

2012 ◽  
Vol 30 (8) ◽  
pp. 628-628
Author(s):  
Cécile Charrier ◽  
Kaumudi Joshi ◽  
Takayuki Sassa ◽  
Jaeda Coutinho‐Budd ◽  
Nelle Lambert ◽  
...  
Keyword(s):  
Gene Duplication ◽  
Brain Development ◽  
Specific Gene ◽  
Human Specific

A Variant Noncoding Region Regulates Prrx1 and Predisposes to Atrial Arrhythmias

2021 ◽  
Author(s):  
Fernanda M Bosada ◽  
Mathilde R Rivaud ◽  
Jae-Sun Uhm ◽  
Sander Verheule ◽  
Karel van Duijvenboden ◽  
...  
Keyword(s):  
Sodium Current ◽  
Association Studies ◽  
Noncoding Region ◽  
Specific Gene ◽  
Genome Wide Association Studies ◽  
Enhancer Activity ◽  
Atrial Cardiomyocytes ◽  
The Impact ◽  
Lineage Specific Gene

Rationale: Atrial Fibrillation (AF) is the most common cardiac arrhythmia diagnosed in clinical practice. Genome-wide association studies have identified AF-associated common variants across 100+ genomic loci, but the mechanism underlying the impact of these variant loci on AF susceptibility in vivo has remained largely undefined. One such variant region, highly associated with AF, is found at 1q24, close to PRRX1, encoding the Paired Related Homeobox 1 transcription factor. Objective: To identify the mechanistic link between the variant region at 1q24 and AF predisposition. Methods and Results: The mouse orthologue of the noncoding variant genomic region (R1A) at 1q24 was deleted using CRISPR genome editing. Among the genes sharing the topologically associated domain with the deleted R1A region (Kifap3, Prrx1, Fmo2, Prrc2c), only the broadly expressed gene Prrx1 was downregulated in mutants, and only in cardiomyocytes. Expression and epigenetic profiling revealed that a cardiomyocyte lineage-specific gene program (Mhrt, Myh6, Rbm20, Tnnt2, Ttn, Ckm) was upregulated in R1A-/- atrial cardiomyocytes, and that Mef2 binding motifs were significantly enriched at differentially accessible chromatin sites. Consistently, Prrx1 suppressed Mef2-activated enhancer activity in HL-1 cells. Mice heterozygous or homozygous for the R1A deletion were susceptible to atrial arrhythmia induction, had atrial conduction slowing and more irregular RR intervals. Isolated R1A-/- mouse left atrial cardiomyocytes showed lower action potential upstroke velocities and sodium current, as well as increased systolic and diastolic calcium concentrations compared to controls. Conclusions: The noncoding AF variant region at 1q24 modulates Prrx1 expression in cardiomyocytes. Cardiomyocyte-specific reduction of Prrx1 expression upon deletion of the noncoding region leads to a profound induction of a cardiac lineage-specific gene program and to propensity for AF. These data indicate that AF-associated variants in humans may exert AF predisposition through reduced PRRX1 expression in cardiomyocytes.

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