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PubMed2004

The roles of segmental and tandem gene duplication in the evolution of large gene families in Arabidopsis thaliana.

BACKGROUND: Most genes in Arabidopsis thaliana are members of gene families. How do the members of gene families arise, and how are gene family copy numbers maintained? Some gene families may evolve primarily through tandem duplication and high rates of birth and death in clusters, and others through infrequent polyploidy or large-scale segmental duplications and subsequent losses. RESULTS: Our approach to understanding the mechanisms of gene family evolution was to construct phylogenies for 50 large gene families in Arabidopsis thaliana, identify large internal segmental duplications in Arabidopsis, map gene duplications onto the segmental duplications, and use this information to identify which nodes in each phylogeny arose due to segmental or tandem duplication. Examples of six gene families exemplifying characteristic modes are described. Distributions of gene family sizes and patterns of duplication by genomic distance are also described in order to characterize patterns of local duplication and copy number for large gene families. Both gene family size and duplication by distance closely follow power-law distributions. CONCLUSIONS: Combining information about genomic segmental duplications, gene family phylogenies, and gene positions provides a method to evaluate contributions of tandem duplication and segmental genome duplication in the generation and maintenance of gene families. These differences appear to correspond meaningfully to differences in functional roles of the members of the gene families.

Arabidopsis↗
PubMed2005

After the duplication: gene loss and adaptation in Saccharomyces genomes.

The ancient duplication of the Saccharomyces cerevisiae genome and subsequent massive loss of duplicated genes is apparent when it is compared to the genomes of related species that diverged before the duplication event. To learn more about the evolutionary effects of the duplication event, we compared the S. cerevisiae genome to other Saccharomyces genomes. We demonstrate that the whole genome duplication occurred before S. castellii diverged from S. cerevisiae. In addition to more accurately dating the duplication event, this finding allowed us to study the effects of the duplication on two separate lineages. Analyses of the duplication regions of the genomes indicate that most of the duplicated genes (approximately 85%) were lost before the speciation. Only a small amount of paralogous gene loss (4-6%) occurred after speciation. On the other hand, S. castellii appears to have lost several hundred genes that were not retained as duplicated paralogs. These losses could be related to genomic rearrangements that reduced the number of chromosomes from 16 to 9. In addition to S. castellii, other Saccharomyces sensu lato species likely diverged from S. cerevisiae after the duplication. A thorough analysis of these species will likely reveal other important outcomes of the whole genome duplication.

Adaptation, Physiological↗
PubMed1998

Two sequence-ready contigs spanning the two copies of a 200-kb duplication on human 21q: partial sequence and polymorphisms.

Physical mapping across a duplication can be a tour de force if the region is larger than the size of a bacterial clone. This was the case of the 170- to 275-kb duplication present on the long arm of chromosome 21 in normal human at 21q11.1 (proximal region) and at 21q22.1 (distal region), which we described previously. We have constructed sequence-ready contigs of the two copies of the duplication of which all the clones are genuine representatives of one copy or the other. This required the identification of four duplicon polymorphisms that are copy-specific and nonallelic variations in the sequence of the STSs. Thirteen STSs were mapped inside the duplicated region and 5 outside but close to the boundaries. Among these STSs 10 were end clones from YACs, PACs, or cosmids, and the average interval between two markers in the duplicated region was 16 kb. Eight PACs and cosmids showing minimal overlaps were selected in both copies of the duplication. Comparative sequence analysis along the duplication showed three single-basepair changes between the two copies over 659 bp sequenced (4 STSs), suggesting that the duplication is recent (less than 4 mya). Two CpG islands were located in the duplication, but no genes were identified after a 36-kb cosmid from the proximal copy of the duplication was sequenced. The homology of this chromosome 21 duplicated region with the pericentromeric regions of chromosomes 13, 2, and 18 suggests that the mechanism involved is probably similar to pericentromeric-directed mechanisms described in interchromosomal duplications.

Cell Line↗
PubMed2002

Analysis of potential duplicates in barley gene bank collections using re-sampling of microsatellite data.

Redundant duplication among putative Nordic spring barley material held at 12 gene banks worldwide was studied using 35 microsatellite primer pairs covering the entire barley genome. These microsatellite markers revealed an average of 7.1 alleles per locus, and a range of 1 to 17 different alleles per locus. Similarity of accession name was initially used to partition the 174 repatriated accessions into 36 potential duplicate groups, and one group containing 36 apparently unique or unrelated accessions. This partitioning was efficient to produce a distribution of mainly small average genetic distances within potential duplicate groups compared to distances from the group of unique accessions. However, comparisons within potential duplicate groups still contained large genetic distances of the same size as distances between unique accessions indicating classification errors. A bootstrap approach based on re-sampling of both microsatellite markers and alleles within marker loci was used to test for homogeneity within potential duplicate groups. The test was used in each group for sequential elimination of accessions with a significantly large average genetic distance to identify a homogeneous group. Such genetically homogeneous groups of two or more accessions were identified in 22 among the 36 potential duplicate groups studied. Results from the genetic analysis of some potential duplicate groups supported previous conclusions based on passport data through inclusion of the historically most-original accession in the genetically homogeneous group. In other potential duplicate groups the apparently most-original accession according to passport data was not included in the homogeneous set of accessions, indicating that this most-original accession does not have duplicate accessions in the group. During the present study the largest average genetic distance accepted in any homogeneous group was smaller than the smallest distance declared significant in any group, with a threshold average genetic distance of approximately 0.14. The results are discussed with respect to the identification of duplicate accessions within potential duplicate groups, as well as the elimination of genetic off types in such groups. Furthermore, large barley gene bank collections may be screened for potential duplicates with genetic distances below the suggested threshold of 0.14.

Gene Library↗
PubMed2006

Direct evidence for the role of centrosomally localized p53 in the regulation of centrosome duplication.

Abnormal amplification of centrosomes is the major cause of mitotic defects and chromosome instability in cancer cells. Centrosomes duplicate once in each cell cycle, and abrogation of the regulatory mechanism underlying centrosome duplication leads to centrosome amplification. p53 tumor suppressor protein is involved in the regulation of centrosome duplication: loss of p53 as well as expression of certain p53 mutants result in deregulated centrosome duplication and centrosome amplification. p53 at least in part depends on its transactivation function to control centrosome duplication, primarily via upregulation of p21 cyclin-dependent kinase (CDK) inhibitor, which prevents untimely activation of CDK2/cyclin E, a key initiator of centrosome duplication. However, numerous studies have shown the presence of p53 at centrosomes, yet the role of the centrosomally localized p53 in the regulation of centrosome duplication had been enigmatic. Here, we comparatively examined wild-type p53 and p53 mutants that are transactivation(+)/centrosome-binding(-), transactivation(-)/centrosome-binding(+) and transactivation(-)/centrosome-binding(-) for their abilities to control centrosome duplication. We found that the transactivation(+)/centrosome-binding(-) and transactivation(-)/centrosome-binding(+) mutants suppress centrosome duplication only partially compared with wild-type p53. Moreover, the transactivation(-)/centrosome-binding(-) mutant almost completely lost the ability to suppress centrosome duplication. These observations provide direct evidence for the centrosomally localized p53 to participate in the regulation of centrosome duplication in a manner independent of its transactivation function in addition to its transactivation-dependent regulation of centrosome duplication.

Animals↗
PubMed1994

Invasion and maintenance of a gene duplication.

The ubiquity of multigene families is evidence for the frequent occurrence of gene duplication, but the origin of multigene families from a single gene remains a little-studied aspect of genome evolution. Although it is clear that a duplication can arise and become fixed in a population purely by random genetic drift and that the rate of fixation is accelerated if the duplication is directly advantageous, the nature of gene duplication suggests that other factors may influence the fate of a novel duplication. In the face of disadvantageous loss-of-function mutations, duplication of a functional gene may provide a buffer against such mutations. Here the conditions for invasion of a rare duplication starting from a mutation-selection balance are derived with formal population genetic models in both haploids and diploids. Recurrent duplication protects the duplicated chromosome from loss and can be very effective in increasing its frequency in a population. In the absence of recurrent duplication, one might suppose that a duplication would be favored by natural selection because it can mask the effects of deleterious mutations. However, the models show that a duplication can invade only if it provides a direct advantage to the organism. This result is closely related to recent theoretical work on the evolution of ploidy.

Diploidy↗
PubMed1998

Pelizaeus-Merzbacher disease: identification of Xq22 proteolipid-protein duplications and characterization of breakpoints by interphase FISH.

Pelizaeus-Merzbacher disease (PMD) is an X-linked, dysmyelinating disorder of the CNS. Duplications of the proteolipid protein (PLP) gene have been found in a proportion of patients, suggesting that, in addition to coding-region or splice-site mutations, overdosage of the gene can cause PMD. We show that the duplication can be detected by interphase FISH, using a PLP probe in five patients and their four asymptomatic carrier mothers. The extent of the duplication was analyzed in each family by interphase FISH, with probes from a 1. 7-Mb region surrounding the PLP gene between markers DXS83 and DXS94. A large duplication >=500 kb was detected, with breakpoints that differed, between families, at the proximal end. Distinct separation of the duplicated PLP signals could be seen only on metaphase chromosomes in one family, providing further evidence that different duplication events are involved. Quantitative fluorescent multiplex PCR was used to confirm the duplication in patients, by the detection of increased copy number of the PLP gene. Multiallelic markers from the duplicated region were analyzed, since the identification of two alleles in an affected boy would indicate a duplication. The majority of boys were homozygous for all four markers, compared with their mothers, who were heterozygous for one to three of the markers. These results suggest that intrachromosomal rearrangements may be a common mechanism by which duplications arise in PMD. One boy was heterozygous for the PLP marker, indicating a duplication and suggesting that interchromosomal rearrangements of maternal origin also can be involved. Since duplications are a major cause of PMD, we propose that interphase FISH is a reliable method for diagnosis and identification of female carriers.

Central Nervous System Diseases↗
PubMed1996

Tandem duplications and large-scale deletions of mitochondrial DNA are early molecular events of human aging process.

Large-scale deletions and tandem duplications of mtDNA, which were originally identified in the patients with KSS or CPEO, have recently been found, although with lower abundance, in various tissues of aged individuals. By use of PCR techniques with back-to-back primers, we demonstrated for the first time that small tandem duplications occur in the D-loop of mtDNA in an age-dependent manner in human tissues. A total of 10 types of such tandem duplications were identified and confirmed by primer-shift PCR and DNA sequencing. Based on the sequence characteristics of the junction sites, we classified these small tandem duplications into 3 groups. Most of the tandem duplications were found to occur at hot spots containing poly C runs, and the number of C residues exhibited wide variations in type I, II, V, VI, VII, and VIII duplications. These observations suggest that these tandem duplications may be generated through similar recombination mechanisms. Among them, type I, II, III, IV and IX duplications were found to occur more frequently and abundantly in aging human tissues. They were not detectable in muscle, testis or skin tissues of young subjects or blood cells from subjects of any age. On the other hand, we also analyzed the samples for the aging-associated 4,977-bp and 7,436-bp mtDNA deletions. The results showed that these two deletions and some of the small tandem duplications could occur alone or in different combinations in human tissues in the aging process. From our data, no clear association between tandem duplications and large-scale deletions of mtDNA could be established. However, one common and important observation is that the incidence and abundance of some of the tandem duplications as well as the large-scale deletions were increased in an age-dependent manner. On the basis of these findings and data reported from this and other laboratories, we propose that tandem duplications and large-scale deletions of mtDNA are early molecular events of the human aging process.

Adolescent↗
PubMed1996

Duplicate laboratory orders: a College of American Pathologists Q-Probes study of thyrotropin requests in 502 institutions.

OBJECTIVE: To examine the frequency and cause of duplicate thyrotropin (TSH) testing. METHODS: Five hundred two institutions, ranging in size from fewer than 100 to more than 600 beds, examined consecutively processed TSH assays to identify duplicate orders. Duplicates were defined as two or more TSH tests performed within 7 days. All together, participants submitted data on 221,476 TSH orders. RESULTS: The median institution reported that 1.5% of TSH tests duplicated a TSH order that had been received from the same patient within the previous 7 days. Ten percent of institutions reported that 4.5% or more of their TSH tests were duplicates. Institutions with higher duplicate rates tended to be larger (ie, they had a greater number of occupied beds) and to have duplicate tests that were more likely to be ordered by a physician other than the one who ordered the initial test. Participants reported that for 19% of duplicate orders, physicians were unaware that the first test had been ordered. Physicians also indicated that duplicate assays were ordered to see if a previous result had changed (15%) or to check on the accuracy of a previous result (13%). Participants reported that 11% of duplicate TSH assays that their laboratory performed had apparently never been ordered. CONCLUSIONS: A large number of institutions are performing duplicate TSH tests that, in most cases, appear to be medically unnecessary. Institutions aiming to reduce the frequency of duplicate testing should consider policies that decrease the opportunity for different physicians to order tests on a single patient and should increase the accuracy with which physician orders are transmitted to the laboratory.

Clinical Laboratory Techniques↗
PubMed1995

[Abnormality of PMP-22 gene in Japanese patients with Charcot-Marie-Tooth disease--comparison between Southern blot and polymerase chain reaction analysis in the detection of PMP-22 gene duplication].

We investigated the duplication of the PMP-22 gene in 23 Japanese patients with Charcot-Marie-Tooth disease (CMT) by Southern blot and PCR analysis. To detect duplication of the PMP-22 gene region, PMP-22 cDNA and a polymorphic marker, VAW409R3, located in the region flanking the PMP-22 gene, were used as probes for Southern blot analysis. A marker, 6G1, also located in the PMP-22 flanking region, was amplified using the quantitative PCR method. The signal intensity of the 2.8-kb and 2.7-kb bands of MspI digests probed with VAW409R3 was different in patients with duplication. The ratio of these two bands, measured by densitometry, ranged from 1.75 to 2.13 in the patients with duplication and from 1.01 to 1.15 in those without duplication and in normal controls. The signal ratio of PMP-22 to the reference marker SF85 of BamHI digests ranged from 1.15 to 1.33 in the patients with duplication and from 0.96 to 1.04 in those without duplication, when compared with normal controls assigned a value of 1.0. The ranges of the intensity in these two groups were narrow, but did not overlap. The signal ratio of the PCR products of 6G1 to reference marker D1S80 on quantitative PCR analysis was also measured. The ratio ranged between 1.67 and 2.23 with duplication and between 1.29 and 1.74 without duplication according to the results of Southern blot analysis. However, some patients exhibited overlapping signal intensity in the duplication and non-duplication ranges. Thus, these three methods each has its own advantages and disadvantages in regard to detecting duplication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1996

Alimentary tract duplications.

A total of 17 patients with alimentary tract duplications underwent surgery at National Taiwan University Hospital from 1978 to 1994. Fifteen patients (88%) had gastrointestinal duplication and two (12%) had esophageal duplication. Common presenting symptoms of gastrointestinal duplication were melena and abdominal pain. The ileum was the most common site of duplication. Multiple duplications were seen in three patients. All duplications were cystic, except for one single appendiceal duplication. Ectopic gastric mucosa was detected in nine of the 16 nongastric duplications. One patient with ileal duplication had ectopic pancreatic tissue. Twelve patients received resection of the duplication with a segment of bowel and primary anastomosis, three patients underwent simple excision and two patients had partial resection of the duplication and stripping of the residual mucosa. Two patients had other associated congenital anomalies: one had ventricular septal defect and the other, imperforate anus and malrotation of intestine. There was no operative mortality or morbidity in this series.

Abdominal Pain↗
PubMed2003

Epigenetic silencing may aid evolution by gene duplication.

Gene duplication is commonly regarded as the main evolutionary path toward the gain of a new function. However, even with gene duplication, there is a loss-versus-gain dilemma: most newly born duplicates degrade to pseudogenes, since degenerative mutations are much more frequent than advantageous ones. Thus, something additional seems to be needed to shift the loss versus gain equilibrium toward functional divergence. We suggest that epigenetic silencing of duplicates might play this role in evolution. This study began when we noticed in a previous publication (Lynch M, Conery JS [2000] Science 291:1151-1155) that the frequency of functional young gene duplicates is higher in organisms that have cytosine methylation (H. sapiens, M. musculus, and A. thaliana) than in organisms that do not have methylated genomes (S. cerevisiae, D. melanogaster, and C. elegans). We find that genome data analysis confirms the likelihood of much more efficient functional divergence of gene duplicates in mammals and plants than in yeast, nematode, and fly. We have also extended the classic model of gene duplication, in which newly duplicated genes have exactly the same expression pattern, to the case when they are epigenetically silenced in a tissue- and/or developmental stage-complementary manner. This exposes each of the duplicates to negative selection, thus protecting from "pseudogenization." Our analysis indicates that this kind of silencing (i) enhances evolution of duplicated genes to new functions, particularly in small populations, (ii) is quite consistent with the subfunctionalization model when degenerative but complementary mutations affect different subfunctions of the gene, and (iii) furthermore, may actually cooperate with the DDC (duplication-degeneration-complementation) process.

Animals↗
PubMed2006

On the formation of novel genes by duplication in the Caenorhabditis elegans genome.

Gene duplication is thought to play the singular most important role in the formation of novel genes. The canonical model of gene duplication postulates that novel genes arise in a two-step fashion, namely, (1) the complete duplication of a gene followed by (2) the gradual accumulation of mutations in one or both copies leading to an altered function. It was previously demonstrated that more than 50% of newborn duplicates in Caenorhabditis elegans had unique exons in one or both members of a duplicate pair, indicating that many duplicates are not functionally identical to the progenitor copy at birth. Both partial and chimeric gene duplications contribute to the formation of novel genes. For chimeric duplications, the genomic sources of unique exons are diverse, including genic and intergenic regions, as well as repetitive elements. These novel genes derived from partial and chimeric duplications are equally likely to be transcriptionally active as copies derived from complete duplications of the ancestral gene. Duplication breakpoints in the ancestral copies are uniformly distributed in the genome, ruling out the role of any mechanism that restricts them to a particular type of sequence such as introns. Finally, both intron loss and gain contribute to the differential distribution of introns between two copies.

Animals↗
PubMed2007

Evolution after gene duplication: models, mechanisms, sequences, systems, and organisms.

Gene duplication is postulated to have played a major role in the evolution of biological novelty. Here, gene duplication is examined across levels of biological organization in an attempt to create a unified picture of the mechanistic process by which gene duplication can have played a role in generating biodiversity. Neofunctionalization and subfunctionalization have been proposed as important processes driving the retention of duplicate genes. These models have foundations in population genetic theory, which is now being refined by explicit consideration of the structural constraints placed upon genes encoding proteins through physical chemistry. Further, such models can be examined in the context of comparative genomics, where an integration of gene-level evolution and species-level evolution allows an assessment of the frequency of duplication and the fate of duplicate genes. This process, of course, is dependent upon the biochemical role that duplicated genes play in biological systems, which is in turn dependent upon the mechanism of duplication: whole genome duplication involving a co-duplication of interacting partners vs. single gene duplication. Lastly, the role that these processes may have played in driving speciation is examined.

Animals↗
PubMed2003

Patterns of gene duplication in Saccharomyces cerevisiae and Caenorhabditis elegans.

In this paper we present a new method for detecting block duplications in a genome. It is more stringent than previous ones in that it requires a more rigorous definition of paralogous genes and that it requires the paralogous proteins on the two blocks to be contiguous. In addition, it provides three criterion choices: (1) the same composition (i.e., having the same paralogues in the two windows), (2) the same composition and gene order, and (3) the same composition, gene order, and gene orientation. The method is completely automated, requiring no visual inspection as in previous methods. We applied it to analyze the complete genomes of S. cerevisiae and C. elegans. In yeast we detected fewer duplicated blocks than previously reported. In C. elegans, however, we detected more block duplications than previously reported, indicating that although our method has a more stringent definition of block duplication than previous ones, it may be more sensitive in detection because it considers every possible window rather than only fixed nonoverlapping windows. Our results show that block duplication is a common phenomenon in both organisms. The patterns of block duplication in the two species are, however, markedly different. The yeast shows much more extensive block duplication than the nematode, with some chromosomes having more than 40% of the duplications derived from block duplications. Moreover, in the yeast the majority of block duplications occurred between chromosomes, while in the nematode most block duplications occurred within chromosomes.

Animals↗
PubMed2005

Gene complexity and gene duplicability.

Eukaryotic genes are on average more complex than prokaryotic genes in terms of expression regulation, protein length, and protein-domain structure [1-5]. Eukaryotes are also known to have a higher rate of gene duplication than prokaryotes do [6, 7]. Because gene duplication is the primary source of new genes [], the average gene complexity in a genome may have been increased by gene duplication if complex genes are preferentially duplicated. Here, we test this "gene complexity and gene duplicability" hypothesis with yeast genomic data. We show that, on average, duplicate genes from either whole-genome or individual-gene duplication have longer protein sequences, more functional domains, and more cis-regulatory motifs than singleton genes. This phenomenon is not a by-product of previously known mechanisms, such as protein function [10-13], evolutionary rate [14, 15], dosage [11], and dosage balance [16], that influence gene duplicability. Rather, it appears to have resulted from the sub-neo-functionalization process in duplicate-gene evolution [11]. Under this process, complex genes are more likely to be retained after duplication because they are prone to subfunctionalization, and gene complexity is regained via subsequent neofunctionalization. Thus, gene duplication increases both gene number and gene complexity, two important factors in the origin of genomic and organismal complexity.

Chromatin Immunoprecipitation↗
PubMedDate not supplied

Divergent origins and concerted expansion of two segmental duplications on chromosome 16.

An unexpected finding of the human genome was the large fraction of the genome organized as blocks of interspersed duplicated sequence. We provide a comparative and phylogenetic analysis of a highly duplicated region of 16p12.2, which is composed of at least four different segmental duplications spanning in excess of 160 kb. We contrast the dispersal of two different segmental duplications (LCR16a and LCR16u). LCR16a, a 20 kb low-copy repeat sequence A from chromosome 16, was shown previously to contain a rapidly evolving novel hominoid gene family (morpheus) that had expanded within the last 10 million years of great ape/human evolution. We compare the dispersal of this genomic segment with a second adjacent duplication called LCR16u. The duplication contains a second putative gene family (KIAA0220/SMG1) that is represented approximately eight times within the human genome. A high degree of sequence identity (approximately 98%) was observed among the various copies of LCR16u. Comparative analyses with Old World monkey species show that LCR16a and LCR16u originated from two distinct ancestral loci. Within the human genome, at least 70% of the LCR16u copies were duplicated in concert with the LCR16a duplication. In contrast, only 30% of the chimpanzee loci show an association between LCR16a and LCR16u duplications. The data suggest that the two copies of genomic sequence were brought together during the chimpanzee/human divergence and were subsequently duplicated as a larger cassette specifically within the human lineage. The evolutionary history of these two chromosome-specific duplications supports a model of rapid expansion and evolutionary turnover among the genomes of man and the great apes.

Animals↗
PubMed2006

Mechanisms and rates of birth and death of dispersed duplicated genes during the evolution of a multigene family in diploid and tetraploid wheats.

A family of 5 genes that evolved within the past 1.9 Myr in diploid wheat was characterized. The ancestral gene, ALP-A1, is on chromosome 1A and encodes an aci-reductone dioxygenase-like protein. The duplicated genes ALP-A2, ALP-A3, ALP-A4.1, and ALP-A4.2 acquired complete coding sequences but lost the original promoter. They are on chromosomes 4A, 2A, 6A and 6A, respectively, and evolved sequentially, the youngest duplicated gene always producing the next duplicate. It is shown that dispersed gene duplication rate consists of the primary rate (duplications of ancestral genes) and the secondary rate (duplications of genes that had been generated by recent duplications). The primary rate was 2.5 x 10(-3) gene(-1) Myr(-1) in diploid wheat. The secondary rate was 5.2 x 10(-2) gene(-1) Myr(-1) in the ALP family. The 20-fold acceleration of the secondary rate was caused by the insertion of the ALP-A2 gene into a novel type transposon. Only the ALP-A1 and ALP-A3 genes are transcribed. The transcription of ALP-A3 is directed by a promoter within a DNA fragment similar to a CACTA type of DNA transposons, making ALP-A3 a new gene. The ALP-A3 transcript is longer than that of the ALP-A1. The half-life of ALP duplicated genes was estimated to be 0.87 Myr. Strong purifying selection acting on the ancestral gene ALP-A1 was undiminished by the evolution of duplicated genes. The evolution of the ALP family shows that repeated elements facilitate both gene duplication and expression of duplicated genes and highlights their importance for the evolution of gene repertoire in large plant genomes.

Amino Acid Sequence↗