scholarly journals Possible role of natural selection in the formation of tandem-repetitive noncoding DNA.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 333-341
Author(s):  
W Stephan ◽  
S Cho

Abstract A simulation model of sequence-dependent amplification, unequal crossing over and mutation is analyzed. This model predicts the spontaneous formation of tandem-repetitive patterns of noncoding DNA from arbitrary sequences for a wide range of parameter values. Natural selection is found to play an essential role in this self-organizing process. Natural selection which is modeled as a mechanism for controlling the length of a nucleotide string but not the sequence itself favors the formation of tandem-repetitive structures. Two measures of sequence heterogeneity, inter-repeat variability and repeat length, are analyzed in detail. For fixed mutation rate, both inter-repeat variability and repeat length are found to increase with decreasing rates of (unequal) crossing over. The results are compared with data on micro-, mini- and satellite DNAs. The properties of minisatellites and satellite DNAs resemble the simulated structures very closely. This suggests that unequal crossing over is a dominant long-range ordering force which keeps these arrays homogeneous even in regions of very low recombination rates, such as at satellite DNA loci. Our analysis also indicates that in regions of low rates of (unequal) crossing over, inter-repeat variability is maintained at a low level at the expense of much larger repeat units (multimeric repeats), which are characteristic of satellite DNA. In contrast, the microsatellite data do not fit the proposed model well, suggesting that unequal crossing over does not act on these very short tandem arrays.

1981 ◽  
Vol 37 (2) ◽  
pp. 133-149 ◽  
Author(s):  
Tomoko Ohta

SUMMARYIn order to understand the evolution of genetic systems in which two genes are tandemly repeated (small multigene family) such as has been recently found in the haemoglobin α loci of primates, haemoglobin β loci of mouse and rarbit and other proteins, a population genetics approach was used. Special reference was made to the probarility of gene identity (identity coefficient), when unequal crossing-over is continuously occurring as well as random genetic drift, inter-chromosomal recombination and mutation. Two models were studied, cycle and selection models. The former assumes that unequal crossing-over occurs in cycles of duplication and deletion, and that the equilibrium identity coefficients were obtained. The latter is based on more realistic biological phenomena, and in this model it is assumed that natural selection is responsible for eliminating chromosomes with extra or deficient gene dose. Unequal crossing-over, inter-chromosomal recombination and natural selection lead to a duplication-deletion balance, which can then be treated as though it were a cycle model. The basic parameter is the rate of duplication-deletion which is shown to be approximately equal to 2(u + 2β)X, where u is the unequal crossing-over rate, 2β is the inter-chromosomal recombination rate and X is the frequency of chromosomes with three genes or of that with one gene. Genetic variation of the globin gene family, of which gene organization is known in most detail, is discussed in the light of the present analyses.


Genetics ◽  
1981 ◽  
Vol 99 (3-4) ◽  
pp. 555-571
Author(s):  
Tomoko Ohta

ABSTRACT The extent of genetic similarity (in terms of identity coefficients) was investigated among members of a multigene family that is evolving under mutation, unequal crossing over and random genetic drift. The method of KIMURA and OHTA (1979) was used, but the possibility was incorporated that the length of the shift (in terms of the number of genes) involved in unequal crossing over can be more than one gene unit. Extensive numerical analyses show that, at equilibrium, the identity coefficients between two gene members are practically independent of their distance apart on the chromosome when the mean length of the shift at unequal crossing over is more than 10% of the total size of the family. In that case, the approximate treatment by OHTA (1980) is shown to be valid, but when the mean length of the shift is less than IO%, the average identity coefficient at equilibrium is underestimated. In order to clarify the effect of natural selection responsible for keeping the family size stable, Monte Carlo simulation studies were performed. The results indicate that the identity coefficients are not greatly influenced by natural selection on gene family size, particularly when the number of genes shifted is small compared to the family size. In addition, with sufficiently strongselection on family size, unequal crossovers with a large shift (such as with maximum shift of 90% of the family size) become ineffective and almost indisdnguishable from those with a small shift.


Genes ◽  
2019 ◽  
Vol 10 (11) ◽  
pp. 896
Author(s):  
Sarah E. Lower ◽  
Anne-Marie Dion-Côté ◽  
Andrew G. Clark ◽  
Daniel A. Barbash

Repetitive DNAs are ubiquitous in eukaryotic genomes and, in many species, comprise the bulk of the genome. Repeats include transposable elements that can self-mobilize and disperse around the genome and tandemly-repeated satellite DNAs that increase in copy number due to replication slippage and unequal crossing over. Despite their abundance, repetitive DNAs are often ignored in genomic studies due to technical challenges in identifying, assembling, and quantifying them. New technologies and methods are now allowing unprecedented power to analyze repetitive DNAs across diverse taxa. Repetitive DNAs are of particular interest because they can represent distinct modes of genome evolution. Some repetitive DNAs form essential genome structures, such as telomeres and centromeres, that are required for proper chromosome maintenance and segregation, while others form piRNA clusters that regulate transposable elements; thus, these elements are expected to evolve under purifying selection. In contrast, other repeats evolve selfishly and cause genetic conflicts with their host species that drive adaptive evolution of host defense systems. However, the majority of repeats likely accumulate in eukaryotes in the absence of selection due to mechanisms of transposition and unequal crossing over. However, even these “neutral” repeats may indirectly influence genome evolution as they reach high abundance. In this Special Issue, the contributing authors explore these questions from a range of perspectives.


Genetics ◽  
1987 ◽  
Vol 115 (1) ◽  
pp. 207-213 ◽  
Author(s):  
Tomoko Ohta

ABSTRACT By considering the recent finding that unequal crossing over and other molecular interactions are contributing to the evolution of multigene families, a model of the origin of repetitive genes was studied by Monte Carlo simulations. Starting from a single gene copy, how genetic systems evolve was examined under unequal crossing over, random drift and natural selection. Both beneficial and deteriorating mutations were incorporated, and the latter were assumed to occur ten times more frequently than the former. Positive natural selection favors those chromosomes with more beneficial mutations in redundant copies than others in the population, but accumulation of deteriorating mutations (pseudogenes) have no effect on fitness so long as there remains a functional gene. The results imply the following: (1) Positive natural selection is needed in order to acquire gene families with new functions. Without it, too many pseudogenes accumulate before attaining a functional gene family. (2) There is a large fluctuation in the outcome even if parameters are the same. (3) When unequal crossing over occurs more frequently, the system evolves more rapidly. It was also shown, under realistic values of parameters, that the genetic load for acquiring a new gene is not as large as J. B. S. Haldane suggested, but not so small as in a model in which a system for selection started from already redundant genes.


Genome ◽  
2004 ◽  
Vol 47 (4) ◽  
pp. 769-774 ◽  
Author(s):  
Joan Pons

A long repeat unit of the PstI family in Misolampus goudoti (Coleoptera, Tenebrionodae) is characterized in this work. The 30 sequenced units have small differences in length (consensus 1169 bp), but very similar nucleotide composition (mean 61.1% A+T). PstI repeats contain a 36-bp-long inverted repeat at both the 5′ and 3′ ends, with a fully conserved 16-bp-long motif similar to those found in class II transposable elements. However, the transposable-like PstI repeats seems to be defective, since they do not encode for any protein related with transposition. Interestingly, energetically stable hairpins resembled the structure of a miniature interspersed transposable element, suggesting that the PstI satellite DNA family in M. goudoti may have originated from an ancestral active transposable element as also described in Drosophila guanche. The presence of transposable-like structure along with the non-detection of gene conversion or unequal crossing-over events suggest that transposition could be one of the putative molecular mechanisms involved in the strong amplification and (or) homogenization of these repeats. A putative transposition of PstI repeats allowing their genomic mobility also could explain why this satellite is widely distributed to all heterochromatic regions, telomeres, pericentromeric regions, and on the Y chromosome, whereas satellites of other tenebrionids lacking transposable-like structures are restricted only to pericentromeric regions.Key words: transposable elements, MITE, satellite DNA, heterochromatin, telomere, beetle, Tenebrionidae.


1986 ◽  
Vol 47 (3) ◽  
pp. 167-174 ◽  
Author(s):  
Wolfgang Stephan

SummaryIn eukaryotic chromosomes, large blocks of satellite DNA are associated with regions of reduced meiotic recombination. No function of highly repeated, tandemly arranged DNA sequences has been identified so far at the cellular level, though the structural properties of satellite DNA are relatively well known. In studying the joint action of meiotic recombination, genetic drift and natural selection on the copy number of a family of highly repeated DNA (HRDNA), this paper looks at the structure–function debate for satellite DNA from the standpoint of molecular population genetics. It is shown that (i) HRDNA accumulates most probably in regions of near zero crossing over (heterochromatin), and that (ii), due to random genetic drift the effect of unequal crossover on copy numbers is stronger, the smaller the population size. As a consequence, highly repeated sequences are likely to persist longest (over evolutionary times) in small populations. The results are based on a fairly general class of models of unequal crossing over and natural selection which have been treated both analytically and by computer simulation.


2009 ◽  
Vol 35 (5) ◽  
pp. 958-961
Author(s):  
Ji-Hua TANG ◽  
Xi-Qing MA ◽  
Wen-Tao TENG ◽  
Jian-Bing YAN ◽  
Jing-Rui DAI ◽  
...  

Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 727-742 ◽  
Author(s):  
R Frankham ◽  
D A Briscoe ◽  
R K Nurthen

ABSTRACT Abdominal bristle selection lines (three high and three low) and controls were founded from a marked homozygous line to measure the contribution of sex-linked "mutations" to selection response. Two of the low lines exhibited a period of rapid response to selection in females, but not in males. There were corresponding changes in female variance, in heritabilities in females, in the sex ratio (a deficiency of females) and in fitness, as well as the appearance of a mutant phenotype in females of one line. All of these changes were due to bb alleles (partial deficiencies for the rRNA tandon) in the X chromosomes of these lines, while the Y chromosomes remained wild-type bb+. We argue that the bb alleles arose by unequal crossing over in the rRNA tandon.—A prediction of this hypothesis is that further changes can occur in the rRNA tandon as selection is continued. This has now been shown to occur.—Our minimum estimate of the rate of occurrence of changes at the rRNA tandon is 3 × 10-4. As this is substantially higher than conventional mutation rates, the questions of the mechanisms and rates of origin of new quantitative genetic variation require careful re-examination.


Sign in / Sign up

Export Citation Format

Share Document