Presented here are hypothetical findings from studies of heterokaryons formed from seven human xeroderma pigmentosum cell strains: $$\begin{array}{lccccccc} & X P 1 & X P 2 & X P 3 & X P 4 & X P 5 & X P 6 & X P 7 \\ X P 1 & \- & & & & & & \\ X P 2 & \- & \- & & & & & \\ X P 3 & \- & \- & \- & & & & \\ X P 4 & \+ & \+ & \+ & \- & & & \\ X P S & \+ & \+ & \+ & \+ & \- & & \\ X P 6 & \+ & \+ & \+ & \+ & \- & \- & \\ X P 7 & \+ & \+ & \+ & \+ & \- & \- & - \end{array}$$ These data are measurements of the occurrence or nonoccur- rence of unscheduled DNA synthesis in the fused heterokaryon. None of the strains alone shows any unscheduled DNA synthesis. Which strains fall into the same complementation groups? How many different groups are revealed based on these data? What can we conclude about the genetic basis of XP from these data?

Step by step solution

01

Understand the Data

We are given a table representing the findings of different combinations of XP1 to XP7 strains and their ability to exhibit unscheduled DNA synthesis. A '+' sign signifies that unscheduled DNA synthesis occurred, while a '-' sign denotes lack of DNA synthesis.

02

Identify Complementation Groups

To find the complementation groups, we should look for XP strains with the same pattern of '+' and '-' signs throughout the table. - XP1, XP2, and XP3 show the same pattern, indicating they belong to the same complementation group. - XP4 and XP5 also share the same pattern and therefore make up another complementation group. - XP6 and XP7 have the same pattern and thus form the third complementation group.

03

Count the Number of Distinct Groups

Based on the observations made in Step 2, we have identified three distinct complementation groups consisting of the following strains: 1. Group 1: XP1, XP2, XP3 2. Group 2: XP4, XP5 3. Group 3: XP6, XP7

04

Draw Conclusions About the Genetic Basis of XP

The data suggests that at least three different genes play a role in xeroderma pigmentosum, as there are three distinct complementation groups. These different genes may have mutations that lead to the lack of unscheduled DNA synthesis, which plays a role in the development of XP.

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