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I am not a biology student and therefore, need clarification if crossover rate and recombination rate are the same thing. So if the text says 'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing? And if not then what is the difference? Also, is 'per base pair' and 'per locus' the same thing?
Let's start with the second question.
Is 'per base pair' and 'per locus' the same thing?
No, not necessarily. A locus (plur. loci) is a location in the genome. It can be of any size. A locus can be a single base pair or it can be 10 base pairs, or a whole gene or anything you want.
'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing?
Recombination rate and crossover rate are not exactly the same thing!
Let's define two loci. Here is a drawing of two haplotypes (the maternal one and the paternal one). Let's represent the loci on the maternal haplotype with capitalized letters and the loci on the paternal haplotype with lower case letters
Let's Let's say that between these two loci there are on average 0.2 crossover per reproduction. The crossover rate is therefore 0.2.
Let's draw the two haplotypes after crossover(s) in a case with…
… 0 crossover
… 1 crossover
… 2 crossovers
… 3 crossovers
… 4 crossovers
You might see a pattern here! If the number of crossovers is even (including 0), then the association between the two loci is unchanged. If the number of crossovers is odd (including 1), then the association between the two loci is changed.
The recombination rate is the rate at which the association between the two loci is changed. Let $P(n)$, be the probability that there are $n$ crossovers betwee our two loci. The recombination rate is therefore $P(1) + P(3) + P(5) + P(7) + P(9) + P(11) +… $.
To make a long story short, the recombination rate is the rate at which the number of crossovers is odd.
Scientists discover gene controlling genetic recombination rates
During sexual reproduction, chromosomes transmitted via the mother and the father’s gametes (egg and sperm) are shuffled to produce a genetic combination unique to each offspring. In most cases, the chromosomes line up properly and crossover (left panel). The unequal crossover (right panel) occurs because of “selfish DNA” sequences known as transposons, represented here as triangles. When abnormal crossovers occur, chromosomes do not line up properly and important genes may be duplicated or deleted. Credit: University of Rochester illustration / Michael Osadciw
Genetics is a crapshoot. During sexual reproduction, genes from both the mother and the father mix and mingle to produce a genetic combination unique to each offspring. In most cases, the chromosomes line up properly and crossover. In some unlucky cases, however, "selfish DNA" enters the mix, causing abnormal crossovers with deletions or insertions in chromosomes, which can manifest as birth defects.
Scientists have long recognized that the exchange of genetic material by crossing over—known as recombination—is vital to natural selection. Yet some species display far more crossover than others. Why? Researchers hypothesize that crossover rates have evolved to balance the benefits of crossing over with the risks of selfish DNA.
"There's a bit of a mystery being solved now about how certain molecular, biological, and genome phenomena have evolved in response to selfish genetic elements," says Daven Presgraves, a dean's professor of biology at the University of Rochester. "The role of natural selection in an ecological context is essentially a solved problem, but the role of natural selection in response to selfish genetic elements is still being worked out."
Presgraves and Ph.D. candidate Cara Brand recently accomplished an important milestone in learning about these evolutionary dynamics. By studying two species of fruit flies, they discovered a gene, MEI-218, that controls the rate of recombination. In a paper published in Current Biology, they explain how MEI-218 controls differences in the rate of crossing over between species and the evolutionary forces at play.
"This is the first gene I know of that anyone has shown to be responsible for the evolution of recombination rates," Presgraves says.
The team focused on two closely related species of fruit flies—Drosophila melanogaster and its sister species, Drosophila mauritiana—because large differences have evolved in their rates of recombination: D. mauritiana does about 1.5 times more crossing over than D. melanogaster. When they compared genes in the two different species, the researchers found that the DNA sequences of MEI-218 were extraordinarily different.PhD candidate and lead author Cara Brand with various species of fruit flies in her lab in Hutchison Hall. Credit: University of Rochester photo / J. Adam Fenster
The importance of genetic recombination
"Natural selection works best when there's a diversity of genotypes to act upon," says Brand, the lead author of the paper. "Shuffling combinations of alleles through recombination generates the diversity upon which natural selection acts."
Recombination is therefore important for two main reasons:
- Imagine two chromosomes with genes A and B. On one chromosome you might have a "good" (beneficial) A allele and a "bad" (deleterious) B allele. On the other chromosome you might have the opposite a bad A allele and a good B allele. Which chromosome would be a better? "It's a mixed bag where one chromosome can't necessarily outcompete the other," Brand says. "Recombination can shuffle our allele combinations so that one chromosome can end up with the good A and B alleles together, while the other can get the bad A and B alleles together. Now when these chromosomes compete, the two good alleles will win out in future generations."
- We have combinations of alleles that are good in our current environment, but the environment is always changing. The good alleles that are adaptive and healthy now may not be so in the next generation. Recombination can shuffle these combinations of genes so that some will be bad and those offspring will die, but some will be good and these offspring will survive.
"Recombination is important—it's not hard to convince anyone of that—but when we look across different species, we see that the rates of crossing over are different," Brand says. "Why increase or decrease the recombination rate?"
The mystery of natural selection and selfish DNA
There is no single ideal rate or distribution of crossovers, Brand says. Crossovers are necessary to produce viable offspring, but crossing over also has risks. Selfish DNA sequences known as transposons—repetitive genetic elements that do not seem to have benefits to their hosts—are distributed throughout the genome. Transposons are akin to viruses, but instead of injecting themselves in cells, they invade genetic material. If abnormal crossovers occur between transposons in different locations on the chromosomes, the chromosomes do not line up properly and important genes may be duplicated or deleted.
Brand and Presgraves hypothesize that the change in recombination rates between D. mauritiana and D. melanogaster may have evolved because the species have different amounts of transposons in their genomes. The D. melanogaster genome has more transposons than D. mauritiana, so D. melanogaster may therefore have evolved a lower rate of crossing over in order to avoid the higher risk of harmful crossovers between transposons.
This means, then, that the MEI-218 gene is constantly evolving to an ever-changing optimum. The evolution of MEI-218 is similar to genes involved in immunity, Presgraves says. "That should make some intuitive sense because genes involved in immunity are constantly adapting to the changing community pathogens that are challenging us all the time."
Evolutionary biologists refer to these kinds of evolutionary dynamics as "evolutionary arms races" because, through positive natural selection, genes are chasing a constantly changing fitness optimum. "Maybe you just adapted, but a few generations from now you're not at the optimum anymore. You have to evolve again and again and again," Presgraves says.
The MEI-218 gene has so far only been investigated in fruit flies, but the research into recombination has applications for humans. "During meiosis at least one crossover per chromosome, in general, is required to make sure the chromosomes separate properly," Brand says. "Either a lack of crossing over or crossing over in the wrong regions of the genome is what leads to many birth defects like Down Syndrome."
Fine-Scale Crossover Rate Variation on the Caenorhabditis elegans X Chromosome
Meiotic recombination creates genotypic diversity within species. Recombination rates vary substantially across taxa, and the distribution of crossovers can differ significantly among populations and between sexes. Crossover locations within species have been found to vary by chromosome and by position within chromosomes, where most crossover events occur in small regions known as recombination hotspots. However, several species appear to lack hotspots despite significant crossover heterogeneity. The nematode Caenorhabditis elegans was previously found to have the least fine-scale variation in crossover distribution among organisms studied to date. It is unclear whether this pattern extends to the X chromosome given its unique compaction through the pachytene stage of meiotic prophase in hermaphrodites. We generated 798 recombinant nested near-isogenic lines (NILs) with crossovers in a 1.41 Mb region on the left arm of the X chromosome to determine if its recombination landscape is similar to that of the autosomes. We find that the fine-scale variation in crossover rate is lower than that of other model species, and is inconsistent with hotspots. The relationship of genomic features to crossover rate is dependent on scale, with GC content, histone modifications, and nucleosome occupancy being negatively associated with crossovers. We also find that the abundances of 4- to 6-bp DNA motifs significantly explain crossover density. These results are consistent with recombination occurring at unevenly distributed sites of open chromatin.
Keywords: C. elegans crossovers meiosis recombination rate variation.
Copyright © 2016 Bernstein and Rockman.
Overview of the sub-NIL cross…
Overview of the sub-NIL cross design focused on the variable X chromosome region.…
Genotypes within the focal interval…
Genotypes within the focal interval in sub-NILs. Each sub-NIL is illustrated as a…
Crossover distributions between parental crosses…
Crossover distributions between parental crosses on the left and right sides of the…
Significant recombination rate heterogeneity. The…
Significant recombination rate heterogeneity. The histograms show the residual deviance under a model…
Recombination rate heterogeneity along the…
Recombination rate heterogeneity along the C. elegans X chromosome left arm is modest…
Histone modification heat map. The…
Histone modification heat map. The correlation matrix of modifications and the IgG binding…
Sex differences in recombination
Department of Biology, McGill University, 1205 Avenue Docteur Penfield, Montreal, P.Q., H3A 1B1,, Canada and Department of Zoology, South Parks Road, Oxford OX1 3PS, U.K.
Department of Biology, McGill University, 1205 Avenue Docteur Penfield, Montreal, P.Q., H3A 1B1,, Canada and Department of Zoology, South Parks Road, Oxford OX1 3PS, U.K.
Department of Biology, McGill University, 1205 Avenue Docteur Penfield, Montreal, P.Q., H3A 1B1,, Canada and Department of Zoology, South Parks Road, Oxford OX1 3PS, U.K.
One of the stronger empirical generalizations to emerge from the study of genetic systems is that achiasmate meiosis, which has evolved 25–30 times, is always restricted to the heterogametic sex in dioecious species, usually the male. Here we collate data on quantitative sex differences in chiasma frequency from 54 species (4 hermaphroditic flatworms, 18 dioecious insects and vertebrates and 32 hermaphroditic plants) to test whether similar trends hold. Though significant sex differences have been observed within many species, only the Liliaceae show a significant sexual dimorphism in chiasma frequency across species, with more crossing over in embryo mother cells than in pollen mother cells chiasma frequencies are unrelated to sex and gamety in all other higher taxa studied. Further, the magnitude of sexual dimorphism, independent of sign, does not differ among the three main ecological groups (dioecious animals, plants, and hermaphroditic animals), contrary to what would be expected if it reflected sex-specific selection on recombination. These results indicate that the strong trends for achiasmate meiosis do not apply to quantitative sex differences in recombination, and contradict theories of sex-specific costs and benefits. An alternative hypothesis suggests that sex differences may be more-or-less neutral, selection determining only the mean rate of recombination. While male and female chiasma frequencies are more similar than would be expected under complete neutrality, a less absolute form of the hypothesis is more difficult to falsify. In female mice the sex bivalent has more chiasmata for its length than the autosomes, perhaps compensating for the absence of recombination in males. Finally, we observe that chiasma frequencies in males and females are positively correlated across species, validating the use of only one sex in comparative studies of recombination.
During meiosis, synapsis (the pairing of homologous chromosomes) ordinarily precedes genetic recombination.
Genetic recombination is catalyzed by many different enzymes. Recombinases are key enzymes that catalyse the strand transfer step during recombination. RecA, the chief recombinase found in Escherichia coli, is responsible for the repair of DNA double strand breaks (DSBs). In yeast and other eukaryotic organisms there are two recombinases required for repairing DSBs. The RAD51 protein is required for mitotic and meiotic recombination, whereas the DNA repair protein, DMC1, is specific to meiotic recombination. In the archaea, the ortholog of the bacterial RecA protein is RadA.
- regular bacterial recombination, as well as noneffective transfer of genetic material, expressed as or abortive transfer which is any bacterialDNA transfer of the donor cell recipients who have set the incoming DNA as part of the genetic material of the recipient. Abortive transfer was registered in the following transduction and conjugation. In all cases, the transmitted fragment is diluted by the culture growth. 
In eukaryotes, recombination during meiosis is facilitated by chromosomal crossover. The crossover process leads to offspring having different combinations of genes from those of their parents, and can occasionally produce new chimeric alleles. The shuffling of genes brought about by genetic recombination produces increased genetic variation. It also allows sexually reproducing organisms to avoid Muller's ratchet, in which the genomes of an asexual population accumulate genetic deletions in an irreversible manner.
Chromosomal crossover involves recombination between the paired chromosomes inherited from each of one's parents, generally occurring during meiosis. During prophase I (pachytene stage) the four available chromatids are in tight formation with one another. While in this formation, homologous sites on two chromatids can closely pair with one another, and may exchange genetic information. 
Because recombination can occur with small probability at any location along chromosome, the frequency of recombination between two locations depends on the distance separating them. Therefore, for genes sufficiently distant on the same chromosome, the amount of crossover is high enough to destroy the correlation between alleles.
Tracking the movement of genes resulting from crossovers has proven quite useful to geneticists. Because two genes that are close together are less likely to become separated than genes that are farther apart, geneticists can deduce roughly how far apart two genes are on a chromosome if they know the frequency of the crossovers. Geneticists can also use this method to infer the presence of certain genes. Genes that typically stay together during recombination are said to be linked. One gene in a linked pair can sometimes be used as a marker to deduce the presence of another gene. This is typically used in order to detect the presence of a disease-causing gene. 
The recombination frequency between two loci observed is the crossing-over value. It is the frequency of crossing over between two linked gene loci (markers), and depends on the mutual distance of the genetic loci observed. For any fixed set of genetic and environmental conditions, recombination in a particular region of a linkage structure (chromosome) tends to be constant, and the same is then true for the crossing-over value which is used in the production of genetic maps.  
In gene conversion, a section of genetic material is copied from one chromosome to another, without the donating chromosome being changed. Gene conversion occurs at high frequency at the actual site of the recombination event during meiosis. It is a process by which a DNA sequence is copied from one DNA helix (which remains unchanged) to another DNA helix, whose sequence is altered. Gene conversion has often been studied in fungal crosses  where the 4 products of individual meioses can be conveniently observed. Gene conversion events can be distinguished as deviations in an individual meiosis from the normal 2:2 segregation pattern (e.g. a 3:1 pattern).
Recombination can occur between DNA sequences that contain no sequence homology. This can cause chromosomal translocations, sometimes leading to cancer.
B cells of the immune system perform genetic recombination, called immunoglobulin class switching. It is a biological mechanism that changes an antibody from one class to another, for example, from an isotype called IgM to an isotype called IgG.
In genetic engineering, recombination can also refer to artificial and deliberate recombination of disparate pieces of DNA, often from different organisms, creating what is called recombinant DNA. A prime example of such a use of genetic recombination is gene targeting, which can be used to add, delete or otherwise change an organism's genes. This technique is important to biomedical researchers as it allows them to study the effects of specific genes. Techniques based on genetic recombination are also applied in protein engineering to develop new proteins of biological interest.
DNA damages caused by a variety of exogenous agents (e.g. UV light, X-rays, chemical cross-linking agents) can be repaired by homologous recombinational repair (HRR).   These findings suggest that DNA damages arising from natural processes, such as exposure to reactive oxygen species that are byproducts of normal metabolism, are also repaired by HRR. In humans, deficiencies in the gene products necessary for HRR during meiosis likely cause infertility  In humans, deficiencies in gene products necessary for HRR, such as BRCA1 and BRCA2, increase the risk of cancer (see DNA repair-deficiency disorder).
In bacteria, transformation is a process of gene transfer that ordinarily occurs between individual cells of the same bacterial species. Transformation involves integration of donor DNA into the recipient chromosome by recombination. This process appears to be an adaptation for repairing DNA damages in the recipient chromosome by HRR.  Transformation may provide a benefit to pathogenic bacteria by allowing repair of DNA damage, particularly damages that occur in the inflammatory, oxidizing environment associated with infection of a host.
When two or more viruses, each containing lethal genomic damages, infect the same host cell, the virus genomes can often pair with each other and undergo HRR to produce viable progeny. This process, referred to as multiplicity reactivation, has been studied in lambda and T4 bacteriophages,  as well as in several pathogenic viruses. In the case of pathogenic viruses, multiplicity reactivation may be an adaptive benefit to the virus since it allows the repair of DNA damages caused by exposure to the oxidizing environment produced during host infection.  See also reassortment.
Molecular models of meiotic recombination have evolved over the years as relevant evidence accumulated. A major incentive for developing a fundamental understanding of the mechanism of meiotic recombination is that such understanding is crucial for solving the problem of the adaptive function of sex, a major unresolved issue in biology. A recent model that reflects current understanding was presented by Anderson and Sekelsky,  and is outlined in the first figure in this article. The figure shows that two of the four chromatids present early in meiosis (prophase I) are paired with each other and able to interact. Recombination, in this version of the model, is initiated by a double-strand break (or gap) shown in the DNA molecule (chromatid) at the top of the first figure in this article. However, other types of DNA damage may also initiate recombination. For instance, an inter-strand cross-link (caused by exposure to a cross-linking agent such as mitomycin C) can be repaired by HRR.
As indicated in the first figure, above, two types of recombinant product are produced. Indicated on the right side is a “crossover” (CO) type, where the flanking regions of the chromosomes are exchanged, and on the left side, a “non-crossover” (NCO) type where the flanking regions are not exchanged. The CO type of recombination involves the intermediate formation of two “Holliday junctions” indicated in the lower right of the figure by two X shaped structures in each of which there is an exchange of single strands between the two participating chromatids. This pathway is labeled in the figure as the DHJ (double-Holliday junction) pathway.
The NCO recombinants (illustrated on the left in the figure) are produced by a process referred to as “synthesis dependent strand annealing” (SDSA). Recombination events of the NCO/SDSA type appear to be more common than the CO/DHJ type.  The NCO/SDSA pathway contributes little to genetic variation, since the arms of the chromosomes flanking the recombination event remain in the parental configuration. Thus, explanations for the adaptive function of meiosis that focus exclusively on crossing-over are inadequate to explain the majority of recombination events.
Achiasmy is the phenomenon where autosomal recombination is completely absent in one sex of a species. Achiasmatic chromosomal segregation is well documented in male Drosophila melanogaster. Heterochiasmy occurs when recombination rates differ between the sexes of a species.  This sexual dimorphic pattern in recombination rate has been observed in many species. In mammals, females most often have higher rates of recombination. The "Haldane-Huxley rule" states that achiasmy usually occurs in the heterogametic sex. 
Numerous RNA viruses are capable of genetic recombination when at least two viral genomes are present in the same host cell.  RNA virus recombination occurs during reverse transcription and is mediated by the enzyme, reverse transcriptase. Recombination occurs when reverse transcriptase jumps from one virus RNA genome to the other virus RNA genome, resulting in a "template switching" event and a single DNA strand that contains sequences from both viral RNA genomes.  Recombination is largely responsible for RNA virus diversity and immune evasion.  RNA recombination appears to be a major driving force in determining genome architecture and the course of viral evolution among picornaviridae ((+)ssRNA) (e.g. poliovirus).  In the retroviridae ((+)ssRNA)(e.g. HIV), damage in the RNA genome appears to be avoided during reverse transcription by strand switching, a form of recombination.  
Recombination in RNA viruses appears to be an adaptation for coping with genome damage.  Switching between template strands during genome replication, referred to as copy-choice recombination, was originally proposed to explain the positive correlation of recombination events over short distances in organisms with a DNA genome (see first Figure, SDSA pathway).  The forced copy-choice model suggests that reverse transcriptase undergoes template switching when it encounters a nick in the viral RNA sequence. Thus, the forced copy-choice model implies that recombination is required for virus integrity and survival, as it is able to correct for genomic damage in order to create proviral DNA.  Another recombination model counters this idea, and instead proposes that recombination occurs sporadically when the two domains of reverse transcriptase, the RNAse H and the polymerase, differ in their activity speeds. This forces the reverse transcriptase enzyme off of one RNA strand and onto the second. This second model of recombination is referred to as the dynamic choice model.  A study by Rawson et al. determined that both recombination models are correct in HIV-1 recombination, and that recombination is necessary for viral replication. 
Recombination can occur infrequently between animal viruses of the same species but of divergent lineages. The resulting recombinant viruses may sometimes cause an outbreak of infection in humans. 
When replicating its (+)ssRNA genome, the poliovirus RNA-dependent RNA polymerase (RdRp) is able to carry out recombination. Recombination appears to occur by a copy choice mechanism in which the RdRp switches (+)ssRNA templates during negative strand synthesis.  Recombination by RdRp strand switching also occurs in the (+)ssRNA plant carmoviruses and tombusviruses. 
Recombination appears to be a major driving force in determining genetic variability within coronaviruses, as well as the ability of coronavirus species to jump from one host to another and, infrequently, for the emergence of novel species, although the mechanism of recombination in is unclear.  During the first months of the COVID-19 pandemic, such a recombination event was suggested to have been a critical step in the evolution of SARS-CoV-2's ability to infect humans.  SARS-CoV-2's entire receptor binding motif appeared, based on preliminary observations, to have been introduced through recombination from coronaviruses of pangolins.  However, more comprehensive analyses later refuted this suggestion and showed that SARS-CoV-2 likely evolved solely within bats and with little or no recombination.  
Crossover Rate Conclusion
- The crossover rate is the cost of capital at which two projects are of equal net present values (NPV) or with intersecting NPV profiles .
- The crossover rate formula requires two variables: Initial Investments (for the two projects) and Cash Flows (from one period to the next).
- The crossover rate is usually expressed as a percentage.
- The crossover rate is used by companies to know which between two projects is more favorable.
There are two popular and overlapping theories that explain the origins of crossing-over, coming from the different theories on the origin of meiosis. The first theory rests upon the idea that meiosis evolved as another method of DNA repair, and thus crossing-over is a novel way to replace possibly damaged sections of DNA. [ citation needed ] The second theory comes from the idea that meiosis evolved from bacterial transformation, with the function of propagating diversity.  In 1931, Barbara McClintock discovered a triploid maize plant. She made key findings regarding corn's karyotype, including the size and shape of the chromosomes. McClintock used the prophase and metaphase stages of mitosis to describe the morphology of corn's chromosomes, and later showed the first ever cytological demonstration of crossing over in meiosis. Working with student Harriet Creighton, McClintock also made significant contributions to the early understanding of codependency of linked genes.
DNA repair theory Edit
Crossing over and DNA repair are very similar processes, which utilize many of the same protein complexes.   In her report, “The Significance of Responses of the Genome to Challenge”, McClintock studied corn to show how corn's genome would change itself to overcome threats to its survival. She used 450 self-pollinated plants that received from each parent a chromosome with a ruptured end. She used modified patterns of gene expression on different sectors of leaves of her corn plants to show that transposable elements (“controlling elements”) hide in the genome, and their mobility allows them to alter the action of genes at different loci. These elements can also restructure the genome, anywhere from a few nucleotides to whole segments of chromosome. Recombinases and primases lay a foundation of nucleotides along the DNA sequence. One such particular protein complex that is conserved between processes is RAD51, a well conserved recombinase protein that has been shown to be crucial in DNA repair as well as cross over.  Several other genes in D. melanogaster have been linked as well to both processes, by showing that mutants at these specific loci cannot undergo DNA repair or crossing over. Such genes include mei-41, mei-9, hdm, spnA, and brca2. [ citation needed ] This large group of conserved genes between processes supports the theory of a close evolutionary relationship. Furthermore, DNA repair and crossover have been found to favor similar regions on chromosomes. In an experiment using radiation hybrid mapping on wheat's (Triticum aestivum L.) 3B chromosome, crossing over and DNA repair were found to occur predominantly in the same regions.  Furthermore, crossing over has been correlated to occur in response to stressful, and likely DNA damaging, conditions  
Links to bacterial transformation Edit
The process of bacterial transformation also shares many similarities with chromosomal cross over, particularly in the formation of overhangs on the sides of the broken DNA strand, allowing for the annealing of a new strand. Bacterial transformation itself has been linked to DNA repair many times. [ citation needed ] The second theory comes from the idea that meiosis evolved from bacterial transformation, with the function of propagating genetic diversity.  .  Thus, this evidence suggests that it is a question of whether cross over is linked to DNA repair or bacterial transformation, as the two do not appear to be mutually exclusive. It is likely that crossing over may have evolved from bacterial transformation, which in turn developed from DNA repair, thus explaining the links between all three processes.
Meiotic recombination may be initiated by double-stranded breaks that are introduced into the DNA by exposure to DNA damaging agents, [ citation needed ] or the Spo11 protein.  One or more exonucleases then digest the 5’ ends generated by the double-stranded breaks to produce 3’ single-stranded DNA tails (see diagram). The meiosis-specific recombinase Dmc1 and the general recombinase Rad51 coat the single-stranded DNA to form nucleoprotein filaments.  The recombinases catalyze invasion of the opposite chromatid by the single-stranded DNA from one end of the break. Next, the 3’ end of the invading DNA primes DNA synthesis, causing displacement of the complementary strand, which subsequently anneals to the single-stranded DNA generated from the other end of the initial double-stranded break. The structure that results is a cross-strand exchange, also known as a Holliday junction. The contact between two chromatids that will soon undergo crossing-over is known as a chiasma. The Holliday junction is a tetrahedral structure which can be 'pulled' by other recombinases, moving it along the four-stranded structure.
Molecular structure of a Holliday junction.
Molecular structure of a Holliday junction. From PDB: 3CRX .
MSH4 and MSH5 Edit
The MSH4 and MSH5 proteins form a hetero-oligomeric structure (heterodimer) in yeast and humans.    In the yeast Saccharomyces cerevisiae MSH4 and MSH5 act specifically to facilitate crossovers between homologous chromosomes during meiosis.  The MSH4/MSH5 complex binds and stabilizes double Holliday junctions and promotes their resolution into crossover products. An MSH4 hypomorphic (partially functional) mutant of S. cerevisiae showed a 30% genome wide reduction in crossover numbers, and a large number of meioses with non exchange chromosomes.  Nevertheless, this mutant gave rise to spore viability patterns suggesting that segregation of non-exchange chromosomes occurred efficiently. Thus in S. cerevisiae proper segregation apparently does not entirely depend on crossovers between homologous pairs.
The grasshopper Melanoplus femur-rubrum was exposed to an acute dose of X-rays during each individual stage of meiosis, and chiasma frequency was measured.  Irradiation during the leptotene-zygotene stages of meiosis (that is, prior to the pachytene period in which crossover recombination occurs) was found to increase subsequent chiasma frequency. Similarly, in the grasshopper Chorthippus brunneus, exposure to X-irradiation during the zygotene-early pachytene stages caused a significant increase in mean cell chiasma frequency.  Chiasma frequency was scored at the later diplotene-diakinesis stages of meiosis. These results suggest that X-rays induce DNA damages that are repaired by a crossover pathway leading to chiasma formation.
In most eukaryotes, a cell carries two versions of each gene, each referred to as an allele. Each parent passes on one allele to each offspring. An individual gamete inherits a complete haploid complement of alleles on chromosomes that are independently selected from each pair of chromatids lined up on the metaphase plate. Without recombination, all alleles for those genes linked together on the same chromosome would be inherited together. Meiotic recombination allows a more independent segregation between the two alleles that occupy the positions of single genes, as recombination shuffles the allele content between homologous chromosomes.
Recombination results in a new arrangement of maternal and paternal alleles on the same chromosome. Although the same genes appear in the same order, some alleles are different. In this way, it is theoretically possible to have any combination of parental alleles in an offspring, and the fact that two alleles appear together in one offspring does not have any influence on the statistical probability that another offspring will have the same combination. This principle of "independent assortment" of genes is fundamental to genetic inheritance.  However, the frequency of recombination is actually not the same for all gene combinations. This leads to the notion of "genetic distance", which is a measure of recombination frequency averaged over a (suitably large) sample of pedigrees. Loosely speaking, one may say that this is because recombination is greatly influenced by the proximity of one gene to another. If two genes are located close together on a chromosome, the likelihood that a recombination event will separate these two genes is less than if they were farther apart. Genetic linkage describes the tendency of genes to be inherited together as a result of their location on the same chromosome. Linkage disequilibrium describes a situation in which some combinations of genes or genetic markers occur more or less frequently in a population than would be expected from their distances apart. This concept is applied when searching for a gene that may cause a particular disease. This is done by comparing the occurrence of a specific DNA sequence with the appearance of a disease. When a high correlation between the two is found, it is likely that the appropriate gene sequence is really closer. 
Crossovers typically occur between homologous regions of matching chromosomes, but similarities in sequence and other factors can result in mismatched alignments. Most DNA is composed of base pair sequences repeated very large numbers of times.  These repetitious segments, often referred to as satellites, are fairly homogenous among a species.  During DNA replication, each strand of DNA is used as a template for the creation of new strands using a partially-conserved mechanism proper functioning of this process results in two identical, paired chromosomes, often called sisters. Sister chromatid crossover events are known to occur at a rate of several crossover events per cell per division in eukaryotes.  Most of these events involve an exchange of equal amounts of genetic information, but unequal exchanges may occur due to sequence mismatch. These are referred to by a variety of names, including non-homologous crossover, unequal crossover, and unbalanced recombination, and result in an insertion or deletion of genetic information into the chromosome. While rare compared to homologous crossover events, these mutations are drastic, affecting many loci at the same time. They are considered the main driver behind the generation of gene duplications and are a general source of mutation within the genome. 
The specific causes of non-homologous crossover events are unknown, but several influential factors are known to increase the likelihood of an unequal crossover. One common vector leading to unbalanced recombination is the repair of double-strand breaks (DSBs).  DSBs are often repaired using homology directed repair, a process which involves invasion of a template strand by the DSB strand (see figure below). Nearby homologous regions of the template strand are often used for repair, which can give rise to either insertions or deletions in the genome if a non-homologous but complementary part of the template strand is used.  Sequence similarity is a major player in crossover – crossover events are more likely to occur in long regions of close identity on a gene.  This means that any section of the genome with long sections of repetitive DNA is prone to crossover events.
The presence of transposable elements is another influential element of non-homologous crossover. Repetitive regions of code characterize transposable elements complementary but non-homologous regions are ubiquitous within transposons. Because chromosomal regions composed of transposons have large quantities of identical, repetitious code in a condensed space, it is thought that transposon regions undergoing a crossover event are more prone to erroneous complementary match-up  that is to say, a section of a chromosome containing a lot of identical sequences, should it undergo a crossover event, is less certain to match up with a perfectly homologous section of complementary code and more prone to binding with a section of code on a slightly different part of the chromosome. This results in unbalanced recombination, as genetic information may be either inserted or deleted into the new chromosome, depending on where the recombination occurred.
While the motivating factors behind unequal recombination remain obscure, elements of the physical mechanism have been elucidated. Mismatch repair (MMR) proteins, for instance, are a well-known regulatory family of proteins, responsible for regulating mismatched sequences of DNA during replication and escape regulation.  The operative goal of MMRs is the restoration of the parental genotype. One class of MMR in particular, MutSβ, is known to initiate the correction of insertion-deletion mismatches of up to 16 nucleotides.  Little is known about the excision process in eukaryotes, but E. coli excisions involve the cleaving of a nick on either the 5’ or 3’ strand, after which DNA helicase and DNA polymerase III bind and generate single-stranded proteins, which are digested by exonucleases and attached to the strand by ligase.  Multiple MMR pathways have been implicated in the maintenance of complex organism genome stability, and any of many possible malfunctions in the MMR pathway result in DNA editing and correction errors.  Therefore, while it is not certain precisely what mechanisms lead to errors of non-homologous crossover, it is extremely likely that the MMR pathway is involved.
Chapter 7 LearningCurve Activity
In chimpanzees, the frequency of recombination is higher in females than in males, while in humans, the frequency of recombination is higher in males than in females.
In humans, many crossover events occur within recombination hotspots, while in chimpanzees, recombination hotspots do not exist.
In chimpanzees, recombination occurs in both males and females, but in humans, recombination is limited to females and doesn't occur in males.
Anaphase of mitosis and anaphase II of meiosis
rates of crossing over are not uniform.
some multiple crossovers go undetected.
interference increases as the distance between genes increases.
testcross results can't be used to map genes that are far apart.
the frequency of recombination is always 50%.
crossovers occur in about 50% of meioses.
each crossover involves all four chromatids but this only occurs in half the meiotic events.
a test cross between a homozygote and heterozygote produces ½ heterozygous and ½ homozygous progeny.
whether the observed number of progeny in a genetic cross differs significantly from the expected number
the interference among genes
the probability that two genes are linked
the chi-square value for independent assortment
The haplotype is likely to increase in size and include additional loci since the increased recombination will now produce more allelic combinations that will be inherited as a unit.
The haplotype should remain in its original form over time.
The haplotype will be disrupted, and some alleles will no longer be in linkage disequilibrium in future times.
Several new haplotypes will be formed along the length of chromosome 4 by the increased rate of recombination.
Problem: Why do calculations of recombination frequencies between loci that are far apart on chromosomes underestimate the true genetic distance between the loci?A. Chromosomes are much longer than the maximum possible genetic distance of 50 map units.B. There is an increased probability of double crossover events with increasing distance, such that a gamete can maintain the parental genotype after many recombination events.C. Recombination rates are uniform across a chromosome, so genetic distances can be expressed as a proportion of the chromosome's physical length.D. Two genes can exhibit a maximum recombination of 50%, so they can only be a maximum of 50 map units apart.
Following Sturtevant's observation regarding the three genes of Drosophila, it can be seen that recombination frequencies are significant contributors to the construction of a genetic map. In this map, the distances between genes are expressed in map units, with one map unit equivalent to a 1% recombination frequency. Therefore, the farther apart 2 genes are from one another, the larger the map unit value, as well as the recombination frequency.
Why do calculations of recombination frequencies between loci that are far apart on chromosomes underestimate the true genetic distance between the loci?
A. Chromosomes are much longer than the maximum possible genetic distance of 50 map units.
B. There is an increased probability of double crossover events with increasing distance, such that a gamete can maintain the parental genotype after many recombination events.
C. Recombination rates are uniform across a chromosome, so genetic distances can be expressed as a proportion of the chromosome's physical length.
D. Two genes can exhibit a maximum recombination of 50%, so they can only be a maximum of 50 map units apart.
New approaches for better dating
O ne approach is to focus on mutations that arise at a steady rate regardless of sex, age, and species. This may be the case for a special type of mutation that geneticists call CpG transitions by which the C nucleotides spontaneously become T’s. Because CpG transitions mostly do not result from DNA copying errors during cell division, their rates should be mainly independent of life history variables—and presumably more uniform over time.
F ocusing on CpG transitions, geneticists recently estimated the split between humans and chimps to have occurred between 9.3 and 6.5 million years ago, which agrees with the age expected from fossils. While in comparisons across species, these mutations seem to happen more like clockwork than other types, they are still not completely steady.
A nother approach is to develop models that adjust molecular clock rates based on sex and other life history traits. Using this method, researchers calculated a chimp-human divergence consistent with the CpG estimate and fossil dates. The drawback here is that, when it comes to ancestral species, we can’t be sure of life history traits, like age at puberty or generation length, leading to some uncertainty in the estimates.
This is a comparison of chromosome 6 from the 40,000-year-old Oase fossil with that of a present-day human. The blue bands represent segments of Neanderthal DNA from past interbreeding. Oase’s segments are longer because he had a Neanderthal ancestor just 4–6 generations before he lived, based on estimates using the recombination clock. Bridget Alex
T he most direct solution comes from analyses of ancient DNA recovered from fossils. Because the fossil specimens are independently dated by geologic methods, geneticists can use them to calibrate the molecular clocks for a given time period or population.
T his strategy recently resolved the debate over the timing of our divergence with Neanderthals. In 2016, geneticists extracted ancient DNA from 430,000-year-old fossils that were Neanderthal ancestors, after their lineage split from Homo sapiens. Knowing where these fossils belong in the evolutionary tree, geneticists could confirm that for this period of human evolution, the slower molecular clock rate of 0.5吆⁻⁹ provides accurate dates. That puts the Neanderthal–modern human split between 765,000 and 550,000 years ago.
As geneticists sort out the intricacies of molecular clocks and sequence more genomes, we’re poised to learn more than ever about human evolution, directly from our DNA.