"Thousands of injuries occur every day."
Milia said quietly, gazing at a DNA model.
Kana was surprised. "To DNA?"
"Yes. UV light, reactive oxygen, replication errors. DNA is damaged by various factors."
Rei supplemented. "But most are repaired. Without repair mechanisms, life couldn't be maintained."
"Repair mechanisms?"
"Multiple systems work cooperatively," Rei drew a diagram on the whiteboard.
"Broadly divided into base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair."
Kana was overwhelmed. "That many?"
"Different mechanisms work depending on the type of damage."
Milia began explaining. "Base excision repair removes chemically altered bases."
"How?"
"An enzyme called DNA glycosylase recognizes damaged bases and cuts them out."
Rei continued. "For example, cytosine sometimes deaminates to become uracil."
"Uracil is an RNA base," Kana recalled.
"It shouldn't be in DNA. Uracil DNA glycosylase finds and removes it."
"Can it be found?"
"The enzyme moves as if sliding along the double helix, detecting abnormal bases."
Milia added. "When a base is removed, a gap called an AP site forms."
"Then what?"
"AP endonuclease cuts the DNA strand. Polymerase fills in the correct nucleotide. Finally ligase connects it."
Kana was impressed. "Teamwork."
"Exactly. A series of enzymes work in sequence."
Rei explained another mechanism. "Nucleotide excision repair deals with larger damage."
"For example?"
"Thymine dimers from UV light. Adjacent thymines become covalently bonded."
"Is that dangerous?"
"DNA polymerase can't pass through. Replication stops."
Milia drew a diagram. "In this case, a long sequence including before and after the damage site is cut out."
"Long?"
"About 30 base pairs. Not just the damaged base, but the surrounding area is removed together."
"That's wasteful," Kana said.
"For certainty," Rei answered. "Cut it large and fill it with the correct sequence."
"If there's a complementary strand, information isn't lost."
Kana understood. "Because it's double-stranded, it's okay if one side is damaged."
"Exactly. One reason DNA is double-stranded."
Milia continued. "But if both strands are cut?"
"Double-strand break. The most serious damage."
"How to repair?"
"Homologous recombination repair or non-homologous end joining," Rei explained.
"Homologous recombination uses a homologous sequence as template. Accurate but requires a homologous sequence."
"Non-homologous end joining?"
"Directly connects cut ends. Fast but error-prone."
Kana asked. "What if repair fails?"
"It becomes a mutation. Most are harmless, but sometimes cause cancer and such."
Milia said quietly. "That's why repair accuracy is extremely important."
"What if repair enzymes themselves are broken?"
"Leads to hereditary cancer syndromes," Rei answered. "For example, BRCA gene mutations."
"I've heard of that."
"BRCA1 and BRCA2 are involved in homologous recombination repair. Mutations increase breast and ovarian cancer risk."
Kana summarized. "DNA repair consists of invisible heroes."
"Repairing thousands of damages every second," Milia nodded.
"Working quietly without rest."
Rei added. "Thanks to that, genetic information fidelity is maintained."
"Small heroes," Kana murmured. "Guardians inside cells."
Milia touched the model. "Many enzymes cooperate to protect this double helix."
"An invisible battle," Kana said.
"But that battle supports our life," Rei concluded.
The three felt deep respect for the DNA repair activities that continue endlessly inside cells.