The bacteria E. coli might sometimes make us sick, but they have served as a workhorse in science. They teach us about DNA and produce ingredients for drugs and fuel molecules. Now E. coli can claim one more skill: They can store our digital data.

In a report published today in Nature, Harvard researchers demonstrate that it is possible to archive images and movies in the DNA of living E. coli cells.

Researchers are continually developing more efficient ways to store digital data. DNA, the building blocks of life, emerged in the mid-1990s as a potential medium. DNA is, after all, just a code—chemicals symbolized by the letters A, T, G, and C—and it can pack a lot of information into a very small space. 

The idea has gained momentum over the last five years. Harvard scientists in 2012 encoded a book in synthesized DNA, and researchers in March reported that they had stored 200 megabytes of data in it—likely the largest amount yet. Even Microsoft has been storing data in DNA. But until now, no one had encoded data right into a living organism, says Seth Shipman, a neuroscientist at Harvard who led the experiments. “That’s much more difficult,” he says.

Shipman and his colleagues encoded into E. coli’s DNA an image and short movie using the gene editing technology CRISPR. The movie, a 36 x 26-pixel GIF of one of the first moving images ever recorded: a galloping mare named Annie G., by Eadweard Muybridge. Shipman and his colleagues retrieved the image and movie with about 90% accuracy using DNA sequencing technology.

So it can be done. But do we want to store our data in living bacteria? Stock our refrigerators with petri dishes full of family memories? (“Mom, where are my prom videos?” “They’re in the E. coli behind the mustard, dear!”)

Perhaps someone will find a use. But Shipman has other plans for his data-storing bacteria: He aims to use it to record the biological activity of cells. “Right now we give DNA information we do know. We want to record information that we don’t know,” he says.

And what we don’t know a lot about is how our own cells in their earliest stages develop. Humans start out as one power-packed ball of pluripotent stem cells, which can turn into anything: brain cells, organ-specific cells, blood cells. But the timing of the development of those cells is not well understood. A data storage system embedded in cells could give us a chronological record of its activity. 

But first, Shipman needed to test the system with electronic data. He chose a movie because it allowed him to demonstrate that he could track hundreds of events, in order, over time.  

Like many bacteria, E. coli has an excellent internal filing system. A section of its genome, known as CRISPR (clustered, regularly interspaced, short palindromic repeats) runs the show. CRISPR’s job is to grab a piece of DNA from viral invaders and file it in the CRISPR section of its genome, generating a chronological record of invaders.

Shipman’s group imagined that if they made the code for digital information look like that of a virus, E. coli’s CRISPR would be fooled into filing it. 

That’s a clever use for CRISPR. Scientists usually use the system as a method for gene editing. Near the CRISPR section of the genome are genes that code for a family of enzymes called Cas, whose job is to slice through DNA strands. Because of that skill, the Cas enzymes—particularly Cas9—have become the tool of choice for scientists who do gene editing. They attach it to a bit of code that can direct it to any spot in organism’s genome, and there it makes a cut, or edit.  

Instead of sending out Cas enzymes to chop up distant places in the genome, Shipman’s group let the CRISPR system behave like it normally does: as a mechanism for grabbing viral DNA and bringing it home to the CRISPR section of the genome. 

So the group converted the image and movie into short DNA segments that look like fragments of viruses, and, frame by frame, introduced them to the organism. E. coli’s CRISPR system was fooled. It grabbed the fragments and filed them in the order in which they were received. Except instead of getting the code for a virus, E. coli got the code for a movie and an image.

Since E. coli is responsible for at least three foodborne disease outbreaks a year in the US, we feel pretty good about pulling one over on the little suckers. 

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Restoring Hearing With Beams of Light

Gene therapy and optoelectronics could radically upgrade hearing for millions of people

13 min read
A computer graphic shows a gray structure that’s curled like a snail’s shell. A big purple line runs through it. Many clusters of smaller red lines are scattered throughout the curled structure.

Human hearing depends on the cochlea, a snail-shaped structure in the inner ear. A new kind of cochlear implant for people with disabling hearing loss would use beams of light to stimulate the cochlear nerve.

Lakshay Khurana and Daniel Keppeler

There’s a popular misconception that cochlear implants restore natural hearing. In fact, these marvels of engineering give people a new kind of “electric hearing” that they must learn how to use.

Natural hearing results from vibrations hitting tiny structures called hair cells within the cochlea in the inner ear. A cochlear implant bypasses the damaged or dysfunctional parts of the ear and uses electrodes to directly stimulate the cochlear nerve, which sends signals to the brain. When my hearing-impaired patients have their cochlear implants turned on for the first time, they often report that voices sound flat and robotic and that background noises blur together and drown out voices. Although users can have many sessions with technicians to “tune” and adjust their implants’ settings to make sounds more pleasant and helpful, there’s a limit to what can be achieved with today’s technology.

8 channels

64 channels

Since optogenetic therapies are just beginning to be tested in clinical trials, there’s still some uncertainty about how best to make the technique work in humans. We’re still thinking about how to get the viral vector to deliver the necessary genes to the correct neurons in the cochlea. The viral vector we’ve used in experiments thus far, an adeno-associated virus, is a harmless virus that has already been approved for use in several gene therapies, and we’re using some genetic tricks and local administration to target cochlear neurons specifically. We’ve already begun gathering data about the stability of the optogenetically altered cells and whether they’ll need repeated injections of the channelrhodopsin genes to stay responsive to light.

Our roadmap to clinical trials is very ambitious. We’re working now to finalize and freeze the design of the device, and we have ongoing preclinical studies in animals to check for phototoxicity and prove the efficacy of the basic idea. We aim to begin our first-in-human study in 2026, in which we’ll find the safest dose for the gene therapy. We hope to launch a large phase 3 clinical trial in 2028 to collect data that we’ll use in submitting the device for regulatory approval, which we could win in the early 2030s.

We foresee a future in which beams of light can bring rich soundscapes to people with profound hearing loss or deafness. We hope that the optical cochlear implant will enable them to pick out voices in a busy meeting, appreciate the subtleties of their favorite songs, and take in the full spectrum of sound—from trilling birdsongs to booming bass notes. We think this technology has the potential to illuminate their auditory worlds.

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