Skip to content

Follow your curiosity.

Try “brain”, “genomics”, or another subject you follow.

Genomics · The big question

A simpler, cheaper way to read the genetic secrets of single cells

Flexible and high-throughput simultaneous profiling of gene expression and chromatin accessibility in single cells

Editorial illustration for Flexible and high-throughput simultaneous profiling of gene expression and chromatin accessibility in single cells
Editorial illustration

Summary

Every cell in a living organism carries the same DNA, but they perform wildly different jobs because they follow different genetic instructions. To truly understand how specific cells work, scientists need to monitor two things at once. They must track which genes are actively turned on, measured through a technique called RNA-seq, and how physically open or accessible the tightly packed DNA is, measured via ATAC-seq. Running both of these measurements simultaneously in a single cell has traditionally been a complex hurdle.

Now, researchers have introduced a streamlined protocol called easySHARE-seq to clear that hurdle. The new tool allows scientists to simultaneously measure both gene expression and chromatin accessibility within individual cells. By improving upon older techniques, easySHARE-seq manages to capture over 1.5 times more genetic transcripts per cell than comparable methods.

The updated protocol also captures longer stretches of genetic code. It extends the usable sequence length to 300 base pairs, a massive 200 base pair increase over previous iterations. This extra length helps researchers spot tiny genetic variations and analyze signals specific to certain genetic alleles. Better yet, the process cuts costs by eliminating the need for a dedicated sequencing run.

Why it matters.

For the biotechnology sector and genetic researchers, easySHARE-seq provides a highly scalable and cost-efficient tool to decode the inner workings of cells. Cheaper, more detailed cellular profiling could accelerate the discovery of new drug targets by helping researchers map out precisely how diseases manipulate our regulatory genes.

That said, the research comes with an important caveat. The current validation relies on an early-stage proof of concept that analyzed 19,664 cell nuclei specifically from mouse livers. Before this technology can be widely adopted for human medicine, researchers will need to conduct further validation to confirm its accuracy and applicability across diverse human tissues and clinical studies.

From the source

The story in numbers.

Murine liver nuclei profiled
19,664
Usable sequence length
300bp
Increase in transcripts recovered per cell
>1.5 fold
Keep the context

Follow the evidence.

This source is a preprint and has not completed peer review. Its findings are provisional.

Your next discovery.

Keep exploring ↗
Genomics

Swapping RNA for DNA gives CRISPR a powerful new target

The gene-editing tool known as CRISPR has revolutionized biology, traditionally relying on a molecule called guide RNA to direct molecular scissors to a specific piece of DNA. However, researchers have discovered a surprising twist. A specific type of molecular scissors known as a Cas12 nuclease can actually be driven by a different genetic navigator. Instead of using traditional guide RNA, this enzyme can utilize guide DNA. This simple substitution fundamentally changes how the tool behaves in a cell. When scientists swap the guide RNA for guide DNA, the Cas12 nuclease stops targeting DNA and instead switches its focus to targeting RNA. RNA is the genetic messenger that helps carry instructions from our genes to the rest of the cell. By just changing the steering mechanism, scientists can completely redirect the cutting machinery to a brand new molecular target. While this discovery significantly expands the overall versatility of the CRISPR toolkit, it is still very preliminary. The current reports are based on an early-stage perspective and lack the quantitative data, clinical validation, and sample size metrics needed to fully understand how well it works in complex organisms.

Nature Biotechnology1 min read
Genomics

Blood Immune Cells May Drive Spinal Cord Damage in ALS

Amyotrophic lateral sclerosis (ALS) is a severe condition that causes a progressive loss of nerve cells in the brain and spinal cord. While scientists have spent decades studying why these neurons fail, recent research published in Nature Neuroscience points to an unexpected culprit. The study reveals that the immune system is not merely reacting to the disease, but actually acts as an active driver of ALS pathology. To uncover this, researchers used advanced techniques called single-cell and spatial transcriptomic profiling. These tools allow scientists to look at the genetic activity of individual cells and map their exact physical locations in the body. Using these methods, the team observed that immune cells from the bloodstream are infiltrating the central nervous system. Once there, these immune cells undergo a reprogramming process that directly links changes in the blood to the severe spinal cord damage seen in ALS patients.

Nature Neuroscience1 min read
Genomics

A Domino Effect: How the Immune System Accelerates ALS

Amyotrophic lateral sclerosis, commonly known as ALS, is a devastating disease that gradually destroys the nerve cells responsible for movement. For years, scientists have puzzled over why the condition progresses rapidly in some patients while others survive much longer. Now, researchers at Northwestern University have uncovered a domino-like cascade that helps explain how the disease unfolds. Rather than a single catastrophic event, ALS appears to start with an internal breakdown inside motor neurons involving a toxic buildup of a protein called TDP-43. This initial damage then triggers a secondary, highly destructive response from the body's own immune system. By examining blood and spinal cord samples from hundreds of living and deceased patients, the scientists mapped out exactly where and how this immune reaction occurs. They discovered that inflamed immune cells from the bloodstream travel into the central nervous system, gathering directly at the sites where motor neurons are dying and toxic proteins are accumulating. Patients with the fastest disease progression had the most intense spinal cord inflammation and higher activity in complement genes, which produce proteins that act as the body's first line of immune defense against damage. Interestingly, the study also revealed that this immune response looks different depending on the root cause of the patient's condition. By analyzing the genetic instructions inside individual cells, the researchers found distinct immune patterns when comparing genetic and non-genetic forms of ALS. This suggests that the immune system reacts uniquely to different variations of the disease.

GEN2 min read

A little science goes a long way.

Clear, thoughtful biotech briefings. In your inbox three times a week.

Stay curious. Subscribe free ↗