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A Missing Muscle Protein: Sprinters, Volunteers and Lab Mice

Trace one common gene change from DNA to protein to traits.

Answer Key

Part 1: Gene, protein and sprint data

Read the passage and Table 1. In Table 1, a difference of less than 0.05 s in sprint time or less than 2 cm in jump height is normal variation and does not count as an effect.

The Question After the Physical

1Jalen Torvik runs the 100 m dash for his middle school track team. At his preseason physical, the sports medicine doctor, Dr. Marisa Quenneville, checked his heart, lungs and joints and cleared him to compete. Jalen had a question for her. A teammate had read online that some people are "born without a sprint gene." Was that true?

2Dr. Quenneville explained that muscles contain two main kinds of fibers. Slow fibers keep working for a long time without tiring, which helps in long runs. Fast fibers contract quickly and powerfully, which helps in sprints and jumps, but they tire sooner. Inside fast fibers is a protein called alpha-actinin-3. It helps hold the fiber's strands of protein in place while the fiber pulls hard. Like every protein, it is built from instructions in a gene.

3Each person carries two copies of this gene, one from each parent. The typical version, called R here, holds the full instructions. A common version, called X, has a single changed letter in its DNA. Because of that change, the cell stops building the protein partway through, and the short piece is broken down. A person with two copies of version X makes no alpha-actinin-3 at all. In some groups of people, about one person in five has two X copies, and these people are healthy. A related protein, built from a different gene, does a similar job in their fast fibers.

4Dr. Quenneville showed Jalen results from a sports science lab. The lab tested 120 adult volunteers who all trained with the same running club for a year. Each volunteer ran a timed 30 m sprint and did a standing jump test. The lab also checked each volunteer's gene versions and looked at a tiny sample of fast fibers under a microscope (Table 1). Every volunteer gave permission, and each test was run three times, with the best result kept.

5The same lab bred mice that lack alpha-actinin-3 and compared them with typical mice of the same age and size. Each mouse ran on a slow treadmill until it tired, and a grip test measured how hard its front paws could pull (Table 2).

Table 1: Running Club Volunteers (group averages)
Gene versionsVolunteersAlpha-actinin-330 m sprint (s)Standing jump (cm)
R and R40Normal amount4.6246
R and X50Less, still present4.6545
X and X30None4.8141
1.
Use paragraphs 2 and 3 and Table 1. Sort each statement by the level it describes.
Version X has one changed letter.The fast fibers of X and X volunteers hold no alpha-actinin-3.X and X volunteers ran 30 m more slowly on average.Version R holds the full set of instructions.A short, unfinished piece of the protein is broken down in the cell.X and X volunteers jumped 5 cm less on average.
The gene (DNA)The proteinThe trait
Version X has one changed letter.
Version R holds the full set of instructions.
The fast fibers of X and X volunteers hold no alpha-actinin-3.
A short, unfinished piece of the protein is broken down in the cell.
X and X volunteers ran 30 m more slowly on average.
X and X volunteers jumped 5 cm less on average.
2.
Use Table 1. Compare the R and R group with the X and X group.

On average, the X and X volunteers took 0.19 s longer to run 30 m.

3.
Use Table 1 and the rule above it. What do the results for the R and X group suggest?
  • A. One R copy gives enough of the protein that sprint and jump show no clear effect.
  • B. Carrying one X copy slows a sprinter about as much as carrying two X copies.
  • C. The R and X volunteers trained harder than the others, which made up for their gene change.
  • D. One X copy changes the R copy in the same cell, so these volunteers make no protein.
4.
People with two X copies make no alpha-actinin-3, yet they are healthy. Which explanation fits paragraph 3 best?
  • A. The short piece of protein does the full job, since it is built from most of the gene.
  • B. Their muscles are made of slow fibers alone, so they have no fast fibers that need it.
  • C. A related protein from another gene does a similar job in their fast fibers.
  • D. Their cells repair the changed letter in childhood, so the protein is made in adults.
5.
Based on Table 1, how does having two X copies most likely affect a person in a 100 m sprint race?
  • A. Harmful, since fast fibers without the protein gave slower sprints and lower jumps
  • B. No clear effect, since the X and X sprint time was within 0.05 s of the other groups
  • C. Helpful, since the X and X volunteers had the fewest people and the fastest times
  • D. Harmful, since the X and X volunteers were less healthy than the other volunteers

Part 2: Mice, training and the whole picture

Use paragraph 5, Table 2 and what you found in Part 1.

Table 2: Lab Mice (averages of 20 mice in each group)
MiceAlpha-actinin-3Treadmill run (m)Front-paw grip (N)
TypicalNormal amount1,2001.8
Bred to lack itNone1,6001.6
6.
Use Table 2. Compare the treadmill runs of the two groups of mice.

To the nearest whole percent, the mice that lack the protein ran 33% farther than the typical mice.

7.
Circle the two results that are evidence that the missing protein lowers muscle strength or power.

Mice that lack the protein ran 1,600 m on the treadmill.Mice that lack the protein pulled 1.6 N in the grip test, compared with 1.8 N.R and X volunteers jumped 45 cm, compared with 46 cm for R and R.X and X volunteers jumped 41 cm, compared with 46 cm for R and R.About one person in five has two X copies in some groups of people.

8.
Which conclusion do Table 1 and Table 2 support together?
  • A. The missing protein harms people and mice in each test, though by different amounts.
  • B. The missing protein makes muscles stronger in mice but weaker in people, so the two tables disagree.
  • C. The missing protein appeared in the mice because they were trained to run long distances.
  • D. The missing protein weakens fast pulling, yet in mice it came with longer runs before tiring.
9.
Jalen has an R copy and an X copy. Over eight weeks of hard sprint training, his 30 m time drops from 4.80 s to 4.70 s. What most likely happened?
  • A. Training changed his slow fibers into fast fibers, which changed the DNA inside them.
  • B. Training changed his muscles, but he still has the same R and X copies he was born with.
  • C. Training turned his X copy into an R copy, so his fast fibers now build more of the protein.
  • D. Training added a third copy of the gene to his fast fibers, which made them pull harder.
10.
Use Table 1.

Of the 120 volunteers, 25% had two X copies.

11.
Jalen's teammate says, "Version X is a harmful mutation. Anyone who has two X copies is worse off." Do you agree? Write a claim, give evidence from both tables and the passage, and explain your reasoning step by step from the gene to the protein to the trait.

I disagree, because the effect of version X depends on the setting. Version X has one changed letter in the gene, so the cell stops building alpha-actinin-3 and people with two X copies have none of the protein in their fast fibers. For sprinting this is harmful: in Table 1 the X and X volunteers ran 30 m in 4.81 s compared with 4.62 s and jumped 41 cm compared with 46 cm, both bigger than normal variation. But for everyday health it has no clear effect: these people are healthy because a related protein from another gene does a similar job. In Table 2, mice without the protein gripped a little less hard (1.6 N compared with 1.8 N) but ran 1,600 m before tiring compared with 1,200 m, so the same change may even help in long, slow exercise. A mutation can change a protein, and the changed protein can change traits, but whether that is harmful, helpful or neither depends on what the body is being asked to do.