Published on: Dec 18, 2025
Scientists at Northwestern Medicine have discovered how molecular “traffic controllers” in cells influence aging and cellular senescence—a state where cells stop dividing but remain metabolically active.
Published in Molecular Cell, the study reveals how transcription elongation factors, including NELF and SPT6, regulate which RNA variants are produced, directly shaping senescence-associated gene programs. Depleting these factors temporarily halts cell growth, but the effect is reversible, suggesting senescence can be modulated.
The team also identified Elongin A (ELOA) as a key regulator of transcription termination, particularly for stress-responsive short genes. Removing ELOA gave aging human fibroblasts a growth advantage, indicating it may act as a molecular brake during aging. Its primate-specific homolog, ELOA3, shows natural variation that could influence susceptibility to age-related diseases.
“These findings reveal a central role for transcription elongation in aging and open new avenues to potentially modulate the process,” said Ali Shilatifard, PhD, senior author of the study.
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