“Good question,” Garlin said. “We’ll get to that. Not only do telomeres protect cells from degrading and losing chromosomes, we found they did other things, much more subtle. By extending the ends of the chromosomes with repetitive, noncoding DNA, they prevent the gradual loss of genetic information that would otherwise result from a quirk in the way DNA is replicated. The polymerase enzyme that copies the DNA can’t reproduce both strands of the double-helical molecule all the way to the ends. As a result, chromosomes would get progressively shorter with every cell division and essential genes would gradually be eroded. This doesn’t happen because the cells can add telomeric DNA to the incompletely replicated ends of the chromosomes.”
“In other words,” Duncan said, “it keeps our gene pool in line.”
“Right. The yeast work showed that when linear DNAs tipped with ciliate telomere sequences are put into yeast cells, they subsequently acquire yeast telomere sequences. This indicated that the yeast was able to add sequences de novo to chromosomes.”
Duncan held up her hand as she tried to follow. “Are you saying the telomere changed to adapt to the new cells?”
“Yes.”
She knew what Garlin was telling her was unusual and she also knew he was leading up to something about what the Grail had done to her.
“Telomerase,” Garlin continued, “is unlike all other enzymes we’ve studied. In addition to protein, it contains an RNA component, which serves as the template for synthesizing the telomere repetitions and the reproduction of the genetic makeup of the host. This suggests that the enzyme might be an intermediate in the evolution from the RNA world to the current world of DNA and protein.” “That’s why unicellular organisms are basically immortal,” she said. “Because they have telomerase, they can replenish their DNA that would otherwise be lost every time the cell divided.”
“Correct,” Garlin said. “And why humans aren’t. Since we don’t have telomerase, our telomeres shorten every time our cells divide. Sperm and egg cells have the longest telomeres. We start dying the second we are conceived and our cells start dividing and multiplying.”
“Why?” Duncan asked.
“That’s the thing that’s puzzled researchers. If a single cell organism can have telomerase, why can’t we? And it’s more than just about dying, we’re also talking about repairing cell damage.”
Duncan’s hand went to her lower chest where Yakov’s bullet had killed her. There was no sign of the wound even though less than a day had passed since she had been shot.
“Telomeres support the activity of the RAD9 gene,” Garlin said. “RAD9 halts the growth of cells whose DNA has been damaged, which suggests that telomeres are part of the cell’s damage-sensing system.”
“So if we could produce the enzyme telomerase,” Duncan said, “we could keep our telomeres active, protect our cells as they reproduce, and be immortal.”
“It’s not that simple,” Garlin said. “Researchers have actually done experiments, trying to make immortal cells. They introduced oncogenes from simian virus 40 into cultured cells to activate telomerase. Many of the cells died, but some survived and continued to divide with active telomerase, which stabilized their telomeres.”
“Why the difference?” Duncan asked.
“There were abnormal chromosomes in the cells that survived. The problem with the research so far,” Garlin continued, “is that, as we told you earlier, the only cells we’ve discovered in humans that have active telomerase are cancer cells. In actuality, most of the medical research in this area so far hasn’t been focused on immortality but on developing inhibitors to block the telomerase in cancer cells so they’ll die.
“Some researchers at the University of Colorado have succeeded in cloning the gene that activates telomerase in human cells. This has led to two hopes — one that we can develop targeted inhibitors that will attack telomerase in cancer while not destroying healthy cells and secondly that we might activate telomerase in healthy cells to slow down aging and cell degeneration.
“We think that telomerase activation may be a necessary step for all tumors. The reason for this is that most cancer cells are immortal. Cancer cells, unlike normal cells, can divide indefinitely in tissue culture if given adequate nutrients. Normal cells have a limit of fifty plus or minus ten divisions, the Hayflick limit, before they grow old in culture and stop dividing. The ability of cancer cells to keep dividing is believed to arise from the activation of telomerase. Therefore if telomerase is inhibited then the telomeres in cancer cells will shorten and will act as a brake on the cancer cell growth.”
“And my telomerase?” Duncan asked. “It’s active.”
“Do I have cancer?”
“No.” Garlin stood. “You’re immortal as far as we can tell. Not only that, but you can replace damaged cells rapidly, as evidenced by your recovery from your gunshot wound.”
“How did this happen?”
“The Grail did something to you,” Garlin said. “We know the end result — your cells actively produce telomerase — but we don’t know how the Grail did this.” He turned for the door. “But we will discover it.”
Artad strode through the main cavern of Qian-Ling, noting the various containers, followed by a half dozen of his kind. The shield generator, a spinning cylinder forty feet long, produced a low hum that pervaded the entire enclosure. He stopped in front of one of the containers right next to the large shield generator and placed his six-fingered hand on a panel. One side slid up, revealing a smaller version of the generator, about ten feet long, resting in a black metal cradle with wheels.
He turned and gestured to his followers. An Airlia got on either side of the generator and moved it out of the container. They followed Artad with it as he continued through the cavern. He paused in front of an intricately designed replica of a dragon — ten meters long, half that wide, with a long arced neck ending at a serpent’s face with dark red eyes. Short wings extended from each side. The metal skin glittered, as bright as the day thousands of years ago that Artad had captured it from Aspasia’s Shadow’s forces. It was known in Chinese lore as Chi Yu, the dragon beast from the south. A ramp, just below the tail, was open, revealing the interior and the pilot’s seat. Artad turned to the Airlia behind him and quickly issued orders in their singsong language. The Arlia and the two pushing the generator went up the ramp. They secured the generator inside and settled down into the seats. The ramp slowly rose and closed.
Using the same drive as the bouncers, Chi Yu rose into the air and turned toward a tunnel that led to the outside world. It disappeared into the tunnel as Artad returned to the room containing the guardian. He turned off the shield wall briefly to allow the flying dragon to depart, then reactivated the wall. He then went over to the guardian and reestablished contact in order to plan the next stages of the war.
Only seventeen miles away. General Kashir could clearly see Mount Ararat directly ahead from his position standing in the top hatch of his armored vehicle. Seventeen miles away and across the border, which was just a quarter mile in front of him. Kashir’s vehicles were on the crest of a small rise, the rest of his column hidden behind him. He could see the border post where a handful of Turkish soldiers were on duty. He had no doubts that he could overrun the post quickly. The issue was what would happen in the seventeen miles on the way to Ararat and then on the slopes of the mountain itself.
He knew that his country was gearing up for war, although the enemy had yet to be determined. There was talk of renewing conflict with Iraq. Others said there would be jihad against Israel, where all the Muslim countries would set aside their differences and destroy the rogue state once and for all. Kashir thought the first was more likely than the second. His mobilization of a mechanized regiment was lost in all the activity and he knew he would not be missed for a while in his own country. The Turks were a different matter.