Microglia, Pol II and ribosomes redrew the flow inside cells
Microglia in ALS mice targeted living motor neurons, Pol II pulled from Drosophila embryos appeared in a stalk-missing elongation form, and ac4C-marked mRNA was read by ribosomes at nearly twice the speed.
Science··Midday
In ALS mice, microglia targeted motor neurons that had not yet died
A Salk Institute team reported that microglia in ALS mice consume motor neurons that are still alive through the receptors Axl and Mer. According to the Medical Xpress summary, muscle control was preserved when those receptors were disabled. The Nature Communications paper frames the sequence as a directly observed cell attack in a widely used ALS mouse model. The result still stops short of showing that the same pathway dominates in human patients. The main weight of the report is that surrounding immune cells may actively shape the damage rather than merely reacting after neurons die.[1]
Pol II pulled directly from embryos showed an elongation form outside the standard diagram
Penn State researchers found an elongation form of RNA polymerase II missing the Rpb4 and Rpb7 subunits after pulling native complexes directly from Drosophila embryos. Phys.org reports that this picture suggests textbook diagrams built from laboratory assemblies may represent the inside of a cell only partially. The Nature Communications paper argues that the gene-reading machine can show a messier and more variable architecture when it is taken from living tissue. The report is less about a new function than about the possibility that the standard structure researchers rely on is incomplete.[2]
ac4C-marked mRNA was read faster and more efficiently by ribosomes
The Johns Hopkins team reported that messenger RNA carrying the ac4C modification was read by ribosomes nearly twice as fast as the m1Ψ-marked form used in COVID-19 vaccines and produced more protein. According to the Phys.org summary, the difference was not limited to speed; output also rose. The Nature paper stays within human and mouse cells, so it does not yet provide a clinical comparison. Read alongside the stalk-missing Pol II elongation form, the result suggests that gene-reading layers may be more variable than the standard diagrams imply.[2], [3]
