Chapter 112. Scientists talk.
Adrian walked into the laboratory quietly, pushing the glass door open with a soft hiss. The familiar sterile scent of ethanol and reagents calmed him. The morning light filtered through the blinds, casting shadows across the counters where test tubes, Petri dishes, and pipettes were neatly arranged. His notebook was already open, with scribbled notes from the night before — mostly DNA sequence variations and molecular pathway diagrams.
He brushed his fingers through his long hair and tucked it behind his ears, glancing at the monitors displaying live tracking of protein expression in the transgenic mice. In the center of the room stood Dr. Zara, dressed in her usual white lab coat, safety glasses pushed onto her head. Her expression was focused as she adjusted the microscope and clicked through fluorescent imaging results.
"You’re up early," Adrian said softly.
Dr. Zara didn’t look up. "Couldn’t sleep. The mice in chamber C3 showed unexpected phenotype expressions." She finally turned toward him, her tone a mix of fatigue and concern. "The formula you created... it’s not perfect yet."
Adrian’s smile faded. "Where exactly is it failing?"
Zara walked over to the main screen and pulled up the data logs. "Here," she pointed to a section of the report. "Your gene-editing solution was meant to stabilize the telomerase overexpression in the modified murine line. But instead of downregulating telomerase, the Cas9 complex triggered off-target effects—particularly on the BRCA2 locus."
Adrian moved closer, eyes scanning the data. "BRCA2... That explains the increased double-strand breaks in the test group."
"Yes," Zara said. "They’re undergoing apoptosis faster than anticipated. We need to reprogram the gRNA. It’s too promiscuous. The sequence you selected overlaps with a pseudogene in the same family — that’s causing the off-target activity."
Adrian pulled his notebook from the table and flipped through the pages. "I cross-checked the guide RNA against the murine genome... but I must’ve missed a partial match in the intronic regions."
Zara nodded. "You’re close, Adrian. But we can’t risk pushing this into the human model without stabilizing these reactions. Especially not when the whole goal is to create a heritable DNA stabilization therapy."
"I thought CRISPR interference with dCas9 might help maintain transcriptional repression," Adrian said. "I used a fusion with KRAB domains to silence the telomerase reactivator sequences."
Zara gave him a sympathetic look. "It did reduce expression—but the epigenetic modifications weren’t stable. Look." She brought up a new slide: chromatin accessibility analysis.