Question

Repressors and Repression How would a mutation in the lexA gene that prevents autocatalytic cleavage of the LexA protein affect the SOS response in \(E\). coli?

Short answer

The mutation would prevent the SOS response, impairing DNA repair.

Step-by-step solution

Understanding the Role of LexA in SOS Response

LexA is a repressor protein that inhibits the expression of SOS genes in normal conditions. During DNA damage, LexA undergoes autocatalytic cleavage initiating the SOS response, allowing for DNA repair and damage tolerance.

Effect of LexA Mutation on Autocatalytic Cleavage

A mutation preventing LexA's cleavage means the protein remains intact and functions as a repressor, continuously blocking SOS gene expression, even following DNA damage.

Impact on SOS Response

Since LexA cannot be cleaved, SOS genes remain repressed. Consequently, the SOS response is unable to activate properly, resulting in impaired DNA repair processes.

Concluding Explanation

In conclusion, the mutation in the lexA gene leads to a failure in initiating the SOS response, due to the continuous repression by the uncleaved LexA protein. This affects the cell's ability to manage DNA damage effectively.

Key concepts

LexA protein

The LexA protein in Escherichia coli is a crucial player in maintaining cellular stability when the DNA is undamaged. It acts as a repressor that binds to specific DNA sequences and inhibits the transcription of SOS genes.
When the cell’s DNA is intact, LexA keeps the SOS system on hold, preventing unnecessary DNA repair activities. However, in the event of DNA damage, this process changes dramatically. The LexA protein undergoes autocatalytic cleavage, a self-cutting action when signaled by another protein known as RecA.
This cleavage is vital because it deactivates LexA’s repressive function, allowing for the transcription of numerous SOS genes. The activation of these genes facilitates cellular DNA repair mechanisms, enabling the cell to recover from potentially damaging situations.

Mutations

Mutations in the lexA gene can significantly affect the effectiveness and efficiency of the SOS response system. A mutation that prevents the autocatalytic cleavage of LexA alters its ability to respond to DNA damage correctly.
Without the ability to cleave, LexA continues to repress SOS gene expression, even when the cell experiences critical DNA damage. This can lead to a cascade of issues:

• Inability to initiate effective DNA repair mechanisms
• Accumulation of unrepaired DNA damage
• Increased susceptibility to mutations in other genes due to the lack of repair and damage tolerance

Such mutations highlight the importance of the LexA cleavage process and its role in maintaining DNA integrity within cells.

DNA repair

DNA repair is an essential physiological process that maintains the integrity and stability of an organism’s genetic material. In bacteria like Escherichia coli, the SOS response is an inducible repair system activated by widespread DNA damage.
Once activated by LexA cleavage, the SOS response facilitates the operation of several DNA repair pathways. These pathways work to fix problems such as broken DNA strands, improper base pairings, and various other DNA lesions. Through

• the induction of error-prone repair mechanisms that allow mutations,
• the recruitment of DNA polymerases specialized in damage tolerance,
• and the activation of recombination processes,

the SOS response attempts to preserve the cell's life by ensuring that damaged DNA is either repaired properly or tolerated until conditions improve.

Repressor proteins

Repressor proteins, like LexA, are essential components of gene regulation systems within cells. They help maintain cellular homeostasis by blocking the expression of specific genes until the organism needs those genes activated.
In the case of LexA, it specifically represses SOS genes responsible for initiating DNA repair and damage tolerance pathways. Importantly, repressors function by binding to operator sequences, small regions of DNA that control the accessibility of transcription machinery to genes.
By understanding the role of LexA as a repressor, it becomes clear that when its function is altered by mutations, the entire balance of gene expression shifts. This can either hinder or facilitate cellular activities that involve a response to DNA damage.