Restriction–Modification Systems—Self-Protection Strategy in Bacteria How do bacterial cells prevent degradation of their own genomic DNA by their resident restriction endonucleases?

Introduction / Context:
Bacterial restriction–modification systems defend against foreign DNA while sparing self-DNA. The restriction enzyme cuts specific sequences, whereas the partner methyltransferase modifies (methylates) those same sequences in the host genome to prevent cleavage.

Given Data / Assumptions:

• Restriction endonucleases recognize short palindromic sequences.
• Each restriction enzyme has an associated DNA methyltransferase with matching specificity.
• Protection must be rapid and site-specific.

Concept / Approach:
Methylation of adenine or cytosine residues within the recognition site alters the enzyme–DNA interaction so that cleavage does not occur on host DNA. Incoming unmethylated foreign DNA (e.g., phage) is cleaved, providing immunity-like protection.

Step-by-Step Solution:

Verification / Alternative check:
Laboratory plasmids often require appropriate methylation patterns to resist specific restriction systems in bacterial hosts, illustrating this mechanism.

Why Other Options Are Wrong:

• Deleting all recognition sites is unrealistic and would be unstable over evolution.
• Not producing nucleases negates defense; not observed in active R–M systems.
• “Anti-restriction endonucleases” is not a standard self-protection mechanism.
• Packaging host DNA into capsids does not occur in bacteria for self-protection.

Common Pitfalls:
Assuming methylation is random; it is exquisitely sequence-specific to match the restriction enzyme.

Final Answer:
They methylate the DNA at the specific recognition sites targeted by the enzyme