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Two theoretical genetic strains of a virus \(\left(a^{-} b^{-} c^{-} \text {and } a^{+} b^{+} c^{+}\right)\) were used to simultaneously infect a culture of host bacteria. Of 10,000 plaques scored, the following genotypes were observed. Determine the genetic map of these three genes on the viral chromosome. Decide whether interference was positive or negative.

Short Answer

Expert verified
Answer: The genetic map for the three genes is ordered as a - 13.1 cM - c - 0.6 cM - b. The interference is negative, as the observed number of double recombinants is greater than the expected number, indicating that one recombination event increases the probability of a second recombination event happening nearby.

Step by step solution

01

Organize the given data

First, we need to tabulate the given data and express it in terms of recombination frequencies. Let's represent the wild type as (+) and the mutant type as (-). Here are the observed genotypes and their occurrences out of 10,000 plaques scored: - a+b+c+: 3,140 - a-b-c-: 3,080 - a+b-c-: 1,740 - a-b+c+: 1,660 - a-b-c+: 675 - a+b-c+: 635 - a+b+c-: 25 - a-b+c-: 35
02

Determine the recombination frequencies

Now, we will calculate the recombination frequency for each possible pair of genes. The recombination frequency is the proportion of recombinant offspring as a result of recombination events between the two genes. - Recombination frequency between a and b: Since a+b-c- and a-b+c- genotypes are recombinants for a and b, we calculate the ratio in the following way: \(\frac{1,740 + 1,660}{10,000} = 0.340\) - Recombination frequency between a and c: Similarly, using the genotypes a-b-c+ and a+b-c+, we calculate: \(\frac{675 + 635}{10,000} = 0.131\) - Recombination frequency between b and c: Using the genotypes a+b+c- and a-b+c-, we calculate: \(\frac{25 + 35}{10,000} = 0.006\)
03

Create the genetic map

To create the genetic map, we multiply each recombination frequency by 100 to convert it to a map distance in centiMorgans (cM). - Map distance between a and b: \(0.340 \times 100 = 34 \text{ cM}\) - Map distance between a and c: \(0.131 \times 100 = 13.1 \text{ cM}\) - Map distance between b and c: \(0.006 \times 100 = 0.6 \text{ cM}\) Since the distance between a and c is smaller than the distance between a and b, we can order the genes as follows: a - c - b. So, the genetic map is: a - 13.1 cM - c - 0.6 cM - b
04

Determine interference

To determine if interference is positive or negative, we need to look at the actual number of double recombinants observed versus the expected number of double recombinants, assuming no interference. The expected number of double recombinants is calculated by multiplying the total number of progeny (10,000) by the product of the recombination frequencies between genes a and c, and genes b and c. Expected double recombinants \( = 10,000 \times 0.131 \times 0.006 = 7.86 \approx 8\) The actual observed number of double recombinants is 25+35=60. Since the observed number of double recombinants (60) is greater than the expected number (8), the interference is negative. This means that the occurrence of one recombination event increases the probability of a second recombination event happening nearby.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Recombination Frequency
Recombination frequency is a crucial concept in genetic mapping. It helps scientists understand how often recombination occurs between two genes during the formation of gametes. Recombination results in the exchange of genetic material between chromosomes, leading to genetic diversity. When measuring recombination frequency, you are essentially identifying how often two genes are separated due to crossovers during meiosis or viral infection cycles in the case of viruses. Understanding Recombination Frequency
Recombination frequency is expressed as a percentage or a decimal and is calculated using the formula:
  • Recombination Frequency = (Number of Recombinant Offspring)/(Total Number of Offspring) × 100%
For example, in the viral experiment provided, one might calculate the recombination frequency between two genes by dividing the number of recombinant viruses by the total number of plaques observed. A higher frequency of recombination suggests that the genes are located farther apart on the chromosome, which means there's more opportunity for a crossover to occur, whereas a lower frequency suggests they are closer together.
Chromosome Mapping
Chromosome mapping, or genetic mapping, is a method used to determine the position of genes on a chromosome. This is done by using recombination frequencies as indicators of the distance between genes. In the exercise, recombination frequencies are translated directly into map distances. This visual representation of gene order is crucial for understanding genetic linkage and for exploring the genetic architecture of organisms. Creating a Genetic Map
To create a genetic map, follow these steps:
  • Calculate recombination frequencies between each pair of genes.
  • Convert these frequencies into map distances by multiplying them by 100 to express them as centiMorgans (cM).
  • Use these distances to arrange the genes, typically in a linear fashion, reflecting their order on the chromosome.
In the provided problem, the genes a, b, and c were mapped in the order of a - 13.1 cM - c - 0.6 cM - b. This arrangement is based on the calculated recombination frequencies between each pair of genes, showing the relative positions on the viral chromosome.
Interference in Genetics
Interference in genetics refers to the phenomenon where the occurrence of one crossover event affects the occurrence of another crossover in its vicinity. Interference can either be positive or negative:
  • Positive interference implies a decrease in the likelihood of another crossover happening nearby, reducing double recombinants.
  • Negative interference suggests an increase in the chance of additional crossovers, leading to more double recombinants than expected.
In our viral genetic mapping exercise, the interference was determined by examining the difference between observed and expected double recombinant frequencies. Analyzing Interference
Calculate expected double recombinants by multiplying individual recombination frequencies:
  • Expected Double Recombinants = Total Progeny × (Recombination Frequency of First Pair) × (Recombination Frequency of Second Pair)
Then, compare this with the observed number of double recombinants. The problem revealed negative interference since the observed double recombinant number was greater than the expected, indicating increased likelihood of nearby crossover events.

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Most popular questions from this chapter

Define plaque, lysogeny, and prophage.

An Hfr strain is used to map three genes in an interrupted mating experiment. The cross is \(H f r / a^{+} b^{+} c^{+} r i f \times F^{-} / a^{-} b^{-} c^{-}\) rif \(^{r} .\) (No map order is implied in the listing of the alleles; rif \(^{r}\) is resistance to the antibiotic rifampicin.) The \(a^{+}\) gene is required for the biosynthesis of nutrient \(\mathrm{A}\), the \(b^{+}\) gene for nutrient \(\mathrm{B}\), and \(c^{+}\) for nutrient \(\mathrm{C}\). The minus alleles are auxotrophs for these nutrients. The cross is initiated at time \(=0\) and at various times, the mating mixture is plated on three types of medium. Each plate contains minimal medium \((\mathrm{MM})\) plus rifampicin plus specific supplements that are indicated in the following table. (The results for each time interval are shown as the number of colonies growing on each plate. (a) What is the purpose of rifampicin in the experiment? (b) Based on these data, determine the approximate location on the chromosome of the \(a, b,\) and \(c\) genes relative to one another and to the F factor. (c) Can the location of the rif gene be determined in this experiment? If not, design an experiment to determine the location of rif relative to the \(\mathrm{F}\) factor and to gene \(b\)

In this chapter, we have focused on genetic systems present in bacteria and on the viruses that use bacteria as hosts (bacteriophages). In particular, we discussed mechanisms by which bacteria and their phages undergo genetic recombination, which allows geneticists to map bacterial and bacteriophage chromosomes. In the process, we found many opportunities to consider how this information was acquired. From the explanations given in the chapter, what answers would you propose to the following questions? (a) How do we know that genes exist in bacteria and bacteriophages? (b) How do we know that bacteria undergo genetic recombination, allowing the transfer of genes from one organism to another? (c) How do we know whether or not genetic recombination between bacteria involves cell-to-cell contact? (d) How do we know that bacteriophages recombine genetic material through transduction and that cell-to-cell contact is not essential for transduction to occur? (e) How do we know that intergenic exchange occurs in bacteriophages? (f) How do we know that in bacteriophage T4 the \(r I I\) locus is subdivided into two regions, or cistrons?

Influenza (the flu) is responsible for approximately 250,000 to 500,000 deaths annually, but periodically its toll has been much higher. For example, the 1918 flu pandemic killed approximately 30 million people worldwide and is considered the worst spread of a deadly illness in recorded history. With highly virulent flu strains emerging periodically, it is little wonder that the scientific community is actively studying influenza biology. In \(2007,\) the National Institute of Allergy and Infectious Diseases completed sequencing of 2035 human and avian influenza virus strains. Influenza strains undergo recombination as described in this chapter, and they have a high mutation rate owing to the error-prone replication of their genome (which consists of RNA rather than DNA). In addition, they are capable of chromosome reassortment in which various combinations of their eight chromosomes (or portions thereof) can be packaged into progeny viruses when two or more strains infect the same cell. The end result is that we can make vaccines, but they must change annually, and even then, we can only guess at what specific viral strains will be prevalent in any given year. Based on the above information, consider the following questions: (a) Of what evolutionary value to influenza viruses are high mutation and recombination rates coupled with chromosome reassortment? (b) Why can't humans combat influenza just as they do mumps, measles, or chicken pox? (c) Why are vaccines available for many viral diseases but not influenza?

Describe how different strains of \(E .\) coli can reveal different linkage arrangements of genes in Hfr crosses.

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