Using CRISPR-Cas9 and adeno-associated virus (AAV)-mediated homology-directed repair, we targeted CAR integration into the endogenous human TCR alpha locus (TRAC). TRAC-CAR T cells display dynamic CAR expression that delays exhaustion and improves tumour control in xenograft and immunocompetent models. This work has been critical for the development of allogeneic CAR T cell therapy, as it disrupts the TCR after transgene insertion—a necessary step to limit graft-versus-host disease.
Young, two-month-old lab mice housed with older, 18-month-old mice showed really impaired cognition. Researchers exposed young mice raised in a sterile, microbe-free environment to gut bacteria from old mice, causing the younger animals to perform worse on cognitive tests, as if they had prematurely aged, just like the cohoused mice.
GEMINI leverages a computationally designed protein assembly as an intracellular memory device to record the history of individual cells. GEMINI grows predictably within live cells, capturing cellular events as tree-ring-like fluorescent patterns for imaging-based retrospective readout. Absolute chronological information of activity histories is attainable with hour-level accuracy.
Fecal transplants from old female mice appear to boost fertility and ovarian health in younger ones. The findings, detailed in a study published Tuesday in the journal Nature Aging, indicate a direct link between gut health and reproductive health in the animals. They could also hold implications for future research into how the microbiome influences ovarian function and fertility in humans.
Scientists have long known that vast colonies of bacteria, viruses and other microorganisms—a population collectively called the microbiome—live on and inside the human body. But how they influenced our health was long a mystery. In just the past few years, we've learned that myriad factors, from the food that we consume to the amount of time that we spend sleeping to our genes to our home, all affect our microbiome.
There are some communities that are very unhealthy where the diversity is higher. Low diversity is not a universal marker. We found something that at first seemed surprising. That a healthy microbiome has lots of competition. These bugs are all going after the same food. In an unhealthy gut, on the other hand, you see tight cooperation - microorganisms are helping each other out.
Biology is undergoing a transformation. After centuries of studying life as it evolves naturally, researchers are now using a combination of computation and genome engineering to intervene, generating new proteins and even whole bacteria from scratch. The use of artificial-intelligence tools to design biological components, an approach known as generative biology, is set to turbocharge this area of research. Just last year, scientists used AI-assisted design to produce artificial genes that can be expressed in mammalian cells.
Gut bacteria are crucial to ensuring healthy digestion and defecation. But two species of bacteria may also be the cause of constipation: according to a new study, Bacteroides thetaiotaomicron and Akkermansia muciniphila appear to work in concert to break down colonic mucin, the slimy coating in our colons that keeps our poo moving along. Too little mucin means a drier and more constipation-prone colon.
The article from the journal argues that the gut-autism axis is a house of cards built on lousy studies with inconsistent data. They assert that the studies are contradictory and that too much emphasis is placed on dubious mouse models. It is notoriously challenging to nail down microbial causes of disease—it is hard enough to simply identify a normal microbiome.
Martschenko's argument is largely that genetic research and data have almost always been used thus far as a justification to further entrench extant social inequalities. But we know the solutions to many of the injustices in our world-trying to lift people out of poverty, for example-and we certainly don't need more genetic research to implement them. Trejo's point is largely that more information is generally better than less.
In Extended Data Fig. 8 of this article, a micrograph shown in the left column (panel AZD) was inadvertently duplicated during figure preparation. The intended image was meant to show phospho-ERK (P-ERK) levels in a MAP2K1-mutant patient-derived xenograft (PDX) exposed to the MEK inhibitor AZD6244 (AZD). However, this image was accidentally overlaid with a micrograph from Extended Data Fig. 10 (left column, panel PAN), which displays P-ERK levels in an EGFR-mutant PDX exposed to panitumumab (PAN).