Building a Paper Model of CRISPR-Cas9

Topic

Resource Type

Level

High School — AP/IB College

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Description

In this hands-on activity, students build a paper model to explore how CRISPR-Cas9 is used to edit genes.

CRISPR-Cas9, commonly referred to as just CRISPR, is often mentioned in the news for its potential to treat genetic diseases. In this activity, students explore and learn about this biotechnology tool by building a two-dimensional paper model of the CRISPR system. They then apply their knowledge of complementary base pairing to model how CRISPR targets specific DNA sequences. Students are asked to compare their paper model to an online three-dimensional model. In an optional extension, students watch and reflect on videos of scientists explaining how they use CRISPR in their research.

The “Resource Google Folder” link directs to a Google Drive folder of resource documents in the Google Docs format. Not all downloadable documents for the resource may be available in this format. The Google Drive folder is set as “View Only”; to save a copy of a document in this folder to your Google Drive, open that document, then select File → “Make a copy.” These documents can be copied, modified, and distributed online following the Terms of Use listed in the “Details” section below, including crediting BioInteractive.

Student Learning Targets

Apply knowledge of DNA structure, function, and base pairing to describe how CRISPR-Cas9 can be used to inactivate and edit genes.
Compare two different models of a biological process.
Explore different types of research projects that apply CRISPR-Cas9 technology (extension).

Estimated Time

One to two 50-minute class periods.

Key Terms

base pairing, complementary sequence, DNA repair, gene editing, gene inactivation, gene knockout, guide RNA, homology-directed repair (HDR), nonhomologous end joining (NHEJ), nuclease

Primary Literature

Ma, Hong, Nuria Marti-Gutierrez, Sang-Wook Park, Jun Wu, Yeonmi Lee, Keiichiro Suzuki, Amy Koski, et al. “Correction of a pathogenic gene mutation in human embryos.” Nature 548, 7668 (2017): 413–419. https://doi.org/10.1038/nature23305.