Genetic studies with heteroduplex DNA of bacteriophage f1. Asymmetric segregation, base correction and implications for the mechanism of genetic recombination

1975 ◽  
Vol 96 (3) ◽  
pp. 495-509 ◽  
Author(s):  
Vincenzo Enea ◽  
Gerald P. Vovis ◽  
Norton D. Zinder
Keyword(s):  
Genetic Recombination ◽  
Genetic Studies ◽  
Heteroduplex Dna

Mismatch repair and the fidelity of genetic recombination

Genome ◽  
1989 ◽  
Vol 31 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Miroslav Radman
Keyword(s):  
Homologous Recombination ◽  
Mismatch Repair ◽  
High Frequency ◽  
Genetic Recombination ◽  
Strand Exchange ◽  
High Fidelity ◽  
Rare Occurrence ◽  
Heteroduplex Dna ◽  
Noncoding Sequences ◽  
Multiple Exchange

Two modes of mismatch repair are known to operate in bacteria: long-patch mismatch repair and very short patch mismatch repair. Very short patch mismatch repair systems act on a specific mismatch by conserving only one base pair. Therefore, when very short patch mismatch repair acts on heteroduplex recombination intermediates, it hyper-recombines specific markers by creating patchwork sequences, i.e., apparent multiple exchange events, on the repaired strand. Long-patch mismatch repair is antirecombinagenic, apparently by decomposing heteroduplex DNA or aborting its formation whenever well-recognized mismatches are formed by strand exchange between nonidentical parental sequences. It is postulated here that mismatch-stimulated antirecombination by long-patch mismatch repair is a "proofreading" system assuring high fidelity of homologous recombination. This accounts for chromosomal stability in eucaryotes (i.e., the rare occurrence of chromosomal aberrations and mitotic recombination versus the high frequency of precise sister chromatid exchange), suggests a role for diverged repetitive and other noncoding sequences as chromosomal antirecombination elements, and provides a molecular mechanism for speciation without the necessity of geographical separation.Key words: mismatch repair, genetic recombination, antirecombination, elements, speciation.

scholarly journals Genetic characterization ofrec-1, a mutant ofUstilago maydisdefective in repair and recombination

1976 ◽  
Vol 27 (3) ◽  
pp. 413-453 ◽  
Author(s):  
R. Holliday ◽  
R. E. Halliwell ◽  
M. W. Evans ◽  
V. Rowell
Keyword(s):  
Genetic Recombination ◽  
Uv Light ◽  
Relative Increase ◽  
Regulatory Function ◽  
Genetic Studies ◽  
Distal Marker ◽  
Recombination Repair ◽  
Spontaneous Frequency ◽  
Size And Morphology ◽  
Mitosis And Meiosis

SUMMARYDetailed physiological and genetic studies of haploid and diploid strains have revealed a complex phenotype for therec-1 mutation inUstilago maydis. The mutant is defective in the repair of damage by UV light, ionizing radiation and nitrosoguanidine. Four alleles are all recessive and have the same sensitivity to UV, suggesting the loss of a single cellular function. A significant fraction of non-viable cells is formed during growth, and in diploid strains considerable variation in colony size and morphology is seen. The spontaneous frequency of mutation is greater than in wild-type cells, but there is little, if any, enhancement by irradiation.rec-1 also has pleiotropic effects on genetic recombination. The spontaneous level of mitotic allelic or non-allelic recombination is abnormally high, but the relative increase after irradiation is much lower than in control diploids. Allelic recombination is strongly associated with the expression of a hetozygous recessive distal marker, and it is shown that this is often due to hemizygosity rather than to homozygosity of this marker. The results indicate that allelic recombination is due to crossing over rather than gene conversion, but that the cross over is often associated with a chromatid break.rec-1 interacts with other radiation sensitive mutants, such asrec-2. Diploids homozygous for both are totally deficient in allelic recombination. In crosses betweenrec-1 strains meiosis is defective, with a low viability of meiotic products and frequent production of aneuploids or diploids among the survivors. The overall phenotype ofrec-1 strains can best be explained in terms of the loss of a regulatory function, which leads to uncontrolled recombination during mitosis and meiosis, and the loss of a recombination repair pathway which is normally induced by agents which damage DNA.

scholarly journals Interaction between mismatch repair and genetic recombination in Saccharomyces cerevisiae.

Genetics ◽  
1994 ◽  
Vol 137 (1) ◽  
pp. 19-39 ◽  
Author(s):  
E Alani ◽  
R A Reenan ◽  
R D Kolodner
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Conversion ◽  
Mismatch Repair ◽  
Base Pair ◽  
Genetic Recombination ◽  
Sequence Similarity ◽  
Amino Acid Sequence Similarity ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
Heteroduplex Dna

Abstract The yeast Saccharomyces cerevisiae encodes a set of genes that show strong amino acid sequence similarity to MutS and MutL, proteins required for mismatch repair in Escherichia coli. We examined the role of MSH2 and PMS1, yeast homologs of mutS and mutL, respectively, in the repair of base pair mismatches formed during meiotic recombination. By using specifically marked HIS4 and ARG4 alleles, we showed that msh2 mutants displayed a severe defect in the repair of all base pair mismatches as well as 1-, 2- and 4-bp insertion/deletion mispairs. The msh2 and pms1 phenotypes were indistinguishable, suggesting that the wild-type gene products act in the same repair pathway. A comparison of gene conversion events in wild-type and msh2 mutants indicated that mismatch repair plays an important role in genetic recombination. (1) Tetrad analysis at five different loci revealed that, in msh2 mutants, the majority of aberrant segregants displayed a sectored phenotype, consistent with a failure to repair mismatches created during heteroduplex formation. In wild type, base pair mismatches were almost exclusively repaired toward conversion rather than restoration. (2) In msh2 strains 10-19% of the aberrant tetrads were Ab4:4. (3) Polarity gradients at HIS4 and ARG4 were nearly abolished in msh2 mutants. The frequency of gene conversion at the 3' end of these genes was increased and was nearly the frequency observed at the 5' end. (4) Co-conversion studies were consistent with mismatch repair acting to regulate heteroduplex DNA tract length. We favor a model proposing that recombination events occur through the formation and resolution of heteroduplex intermediates and that mismatch repair proteins specifically interact with recombination enzymes to regulate the length of symmetric heteroduplex DNA.

Electron Microscopy and image analysis of nucleo-protein complexes

1994 ◽  
Vol 52 ◽  
pp. 88-89
Author(s):  
E. H. Egelman ◽  
X. Yu
Keyword(s):  
Electron Microscopy ◽  
Image Analysis ◽  
Normal Cell ◽  
Genetic Recombination ◽  
Protein Complexes ◽  
Chromosomal Rearrangements ◽  
Reca Protein ◽  
E Coli ◽  
Helical Polymer ◽  
Specific Protease

The RecA protein of E. coli has been shown to mediate genetic recombination, regulate its own synthesis, control the expression of other genes, act as a specific protease, form a helical polymer and have an ATPase activity, among other observed properties. The unusual filament formed by the RecA protein on DNA has not previously been shown to exist outside of bacteria. Within this filament, the 36 Å pitch of B-form DNA is extended to about 95 Å, the pitch of the RecA helix. We have now establishedthat similar nucleo-protein complexes are formed by bacteriophage and yeast proteins, and availableevidence suggests that this structure is universal across all of biology, including humans. Thus, understanding the function of the RecA protein will reveal basic mechanisms, in existence inall organisms, that are at the foundation of general genetic recombination and repair.Recombination at this moment is assuming an importance far greater than just pure biology. The association between chromosomal rearrangements and neoplasms has become stronger and stronger, and these rearrangements are most likely products of the recombinatory apparatus of the normal cell. Further, damage to DNA appears to be a major cause of cancer.

Moving beyond the “LDL hypothesis”

VASA ◽  
2015 ◽  
Vol 44 (5) ◽  
pp. 333-340 ◽  
Author(s):  
Christian Werner ◽  
Ulrich Laufs
Keyword(s):  
Ldl Cholesterol ◽  
Causal Relation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Clinical Trial Data ◽  
Randomised Clinical Trial ◽  
Trial Data ◽  
Low Density Lipoprotein Cholesterol ◽  
Genetic Studies ◽  
Statin Drug

Abstract. Summary: The term “LDL hypothesis” is frequently used to describe the association of low-density lipoprotein cholesterol (LDL-cholesterol, LDL-C) and cardiovascular (CV) events. Recent data from genetic studies prove a causal relation between serum LDL-C and CV events. These data are in agreement with mechanistic molecular studies and epidemiology. New randomised clinical trial data show that LDL-C lowering with statins and a non-statin drug, ezetimibe, reduces CV events. We therefore believe that the “LDL-hypothesis” has been proven; the term appears to be outdated and should be replaced by “LDL causality”.

Neuropsychological intermediate phenotypes as tools for genetic studies in schizophrenia

2009 ◽  
Vol 42 (05) ◽  
Author(s):  
H Konnerth ◽  
I Giegling ◽  
AM Hartmann ◽  
J Genius ◽  
A Ruppert ◽  
...  
Keyword(s):  
Genetic Studies ◽  
Intermediate Phenotypes

The Use of Medical Record Linkage for Population and Genetic Studies

1969 ◽  
Vol 08 (01) ◽  
pp. 07-11 ◽  
Author(s):  
H. B. Newcombe
Keyword(s):  
Record Linkage ◽  
Large Scale ◽  
Medical Record Linkage ◽  
Canadian Province ◽  
Genetic Studies ◽  
Parental Characteristics ◽  
Family Histories ◽  
The Family ◽  
Large Populations ◽  
Machine Readable

Methods are described for deriving personal and family histories of birth, marriage, procreation, ill health and death, for large populations, from existing civil registrations of vital events and the routine records of ill health. Computers have been used to group together and »link« the separately derived records pertaining to successive events in the lives of the same individuals and families, rapidly and on a large scale. Most of the records employed are already available as machine readable punchcards and magnetic tapes, for statistical and administrative purposes, and only minor modifications have been made to the manner in which these are produced.As applied to the population of the Canadian province of British Columbia (currently about 2 million people) these methods have already yielded substantial information on the risks of disease: a) in the population, b) in relation to various parental characteristics, and c) as correlated with previous occurrences in the family histories.

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