New gene editing calls for ways to regulate it
Powerful, new bioscience technologies demand equally powerful policies to manage them.
Effective policies, in turn, require policymakers — and the people who elect them — to understand those technologies and the evolutionary biology behind them.
Last month, the U.S. National Academies of Sciences and of Medicine and the U.K. Royal Society launched an International
Commission to propose guidelines for possible, clinical applications of a new genome editing technology.
The effort responds to the surprise announcement last November that a Chinese biophysicist edited the genome of twin, human embryos.
The father of newly born Lulu and Nana had HIV. The researcher used CRISPR gene editing technology to disable the girls’ CCR5 gene. HIV uses the CCR5 protein to infect human cells. People with naturally occurring—or Crispr-edited—shortened copies of CCR5 generally resist HIV infection.
CRISPR exploits a recently discovered, anti-viral immune enzyme produced by bacteria. In 2012, Jennifer Doudna, a University of California Berkeley biochemist, and colleagues reported how CRISPR can easily edit genomes of most organisms.
CRISPR functions like the “find and replace” function of word processor programs. The Chinese biophysicist used it to find and delete a 32-base section of Lulu’s and Nana’s CCR5 gene.
A single DNA base change in the human-hemoglobin gene causes sickle-cell anemia in people who inherit two copies of the changed gene. Researchers hope CRISPR can find and replace that DNA base with the one found in people without sickle-cell anemia.
So, why the international outrage?
Editing an embryo’s genome can alter that genome in sperm or egg producing cells of the eventual adult. We perform genetic surgery on an embryo and all of its descendants.
CRISPR can alter nontarget sections of a subject’s genome. It can replace a targeted gene segment incorrectly. CRISPR might not alter a gene in all cells of an embryo or targeted tissue leading to unknown effects.
It’s tempting to suggest that CRISPR can rid us and our descendants of “bad genes.”
But from an evolutionary perspective, there are few bad genes. Rather, some “good genes” occur in bad environments. The sickle-cell gene provides malaria resistance to its carriers. As climate change expands the range of malaria, people might not want to “fix” that gene for their descendants.
Calls for guidelines on the use of gene-editing technologies reveal how much we have learned about the biochemistry of DNA bases and the proteins they encode. They also reveal how little we know about how evolution and the environmental influence those genes.
Steve Rissing is a professor in the Department of Evolution, Ecology and Organismal Biology at Ohio State University. steverissing@hotmail.com