Researchers discover new mechanism in TB bacteria functioning

Researchers discover new mechanism in TB bacteria functioning
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In a significant breakthrough for biology and medical research, Indian scientists have uncovered new insights into how bacteria regulate gene expression—findings that could pave the way for improved strategies to combat Tuberculosis (TB), one of the world’s deadliest infectious diseases. For decades, textbooks in Molecular Biology have described a widely accepted mechanism known as the “σ-cycle.”

According to this model, a protein called the sigma (σ) factor binds to RNA polymerase to initiate transcription—the first step of gene expression—and then detaches as the enzyme proceeds to elongate RNA. This process was believed to be universal across all bacteria, including the TB-causing Mycobacterium tuberculosis.

However, a new study by researchers at the Bose Institute, an autonomous institute under the Department of Science and Technology, has challenged this long-standing assumption. The research, led by Jayanta Mukhopadhyay and N. Hazra, reveals that the σ-cycle is not as universal as previously thought.

The team discovered that while some sigma factors detach from RNA polymerase during transcription, others remain bound throughout the process. This finding highlights that different σ factors behave in distinct ways, indicating a more complex regulatory mechanism than earlier understood.

Published in the international journal Nucleic Acids Research, the study focuses specifically on Mycobacterium tuberculosis. It shows that certain sigma factors, such as σF, stay attached to RNA polymerase, enabling the bacterium to maintain continuous expression of genes, especially those required under stress conditions.

This discovery is particularly important in the context of TB, as the bacterium survives within the human body by adapting to harsh environments. Understanding how gene expression is regulated in such conditions could help scientists design more effective treatments, especially against drug-resistant strains.

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