Chapter 7

Over dinner, Dixie listened to Harry relate the details of his meeting with Pauling and Alistair Forester that afternoon. She was appalled that, after several years and thinking this issue had been put to rest, now it would be drudged up again. As she and Harry ate, he recounted the meeting. His description caused her stomach slowly contract into tight knots, and anger boiled in her veins. No one was going to threaten her husband.

“So,” Harry concluded, “I guess I must wait until I hear from the board of trustees and whatever investigation they decide upon. I’m kinda in limbo right now.”

“The bastard,” Dixie seethed, spitting the word out like venom. “Can you count on Pauling for support?”

“I think so. He said as much at the meeting, but he answers to the board. I’m sure he’ll protect his own interests if it comes down to the nitty-gritty. Right now, I feel I’m out on that proverbial limb, and Forester is sawing.”

“I’m for locating that bastard Wickingham and suing his ass off,” Dixie said, her voice still hot with rancor.

“Honey, I’m guilty as charged, remember? I admitted my crime. There’s no libel in that.”

“But it’s over and done with. Years ago. Finished. Even Pauling agreed with that. The only motive Wickingham could have now is character assassination. If the university president is satisfied with you, why can’t the trustees be?”

“It’s all politics. Forester is afraid the university will suffer a downturn in public perception. And that means money. Fewer donations from the big money types.”

“So this is all going to boil down to money?” Dixie’s tone sounded incredulous. “They’re going to throw you under the bus simply for financial reasons?”

“Maybe. We’ll have to wait and see,” Harry said.

“All the same, if Pauling doesn’t support you a hundred percent, I’ll never forgive him.”

“And Professor Kesler,” Harry added, “don’t forget about him.”

“He gave you a second chance. Doesn’t everyone deserve a second chance? His support and recommendation as his successor should count for something. I hope Pauling makes that point clear to the trustees. Harry, have you thought about just resigning?”

“You mean now? Before the investigation?”

“Yes. Now. You can find another position, what with your reputation. I’ll go wherever you want to go.”

“I need to stay and see this through, sweetheart. If I left, this issue would just follow me wherever I went, now that it’s out in the public domain. So I believe now is the time to face this down, once and for all.”

“Wickingham was always such a creep,” Dixie said, her tone somewhat calmer. “He was always leering at the ladies and trying to sneak a peek down our blouses. I had the jitters when he was around.”

“Yeah, even Chloe Rawlings had similar feelings, and you know if she didn’t like someone, they must really be something.”

“I still think we need to consult a lawyer.”

Harry shook his head. “Let’s wait and see how this plays out. Who knows, the trustees may decide in my favor. Forester is only one voice.”

Dixie began clearing the dishes from the table. “And if the investigation goes against you and you get a formal reprimand?”

“Then so be it. I will have done my best.”

***

Two weeks after the embryo transfer, Millie and Siscom reviewed Tika’s latest progesterone blood levels. As they looked over the results a smile formed on Millie’s face.

“The level,” she said, “it’s rising. She’s pregnant!”

“She sure is,” Siscom said. “Now if she can just maintain the pregnancy. That’s the next hurdle.”

“So the progesterone is what maintains the pregnancy?” Millie said. The two were sitting in Siscom’s office.

“Yes,” Siscom said. “It’s the modulating effects of progesterone on endometrial structure and function that are essential to the success of reproduction. After ovulation, progesterone produced by the corpus luteum induces maturation of the endometrium, involving a cascade of molecular events that ultimately renders the endometrium receptive to implantation of the embryo. After that and with continued progesterone stimulation, driven by rapidly increasing concentrations of chorionic gonadotropin, the endometrium is reconfigured to support early embryonic development.”

“What if there’s not enough progesterone?” Millie asked.

“Considering the important role that progesterone plays in reproduction, it is not surprising that exogenous supplemental progesterone is a common element of treatment regimens in infertility, particularly those relating to the assisted reproductive technologies.”

“How so?” Millie said.

“A classic series of studies, conducted more than three decades ago, demonstrated that progesterone secretion by the corpus luteum is absolutely required for the success of early human pregnancy. Surgical excision of the corpus luteum, or luteectomy, before seven weeks’ gestation uniformly precipitated an abrupt decrease in serum progesterone concentrations, followed by miscarriage. When luteectomy was performed more than twenty-seven days after the missed menstrual period, progesterone levels decreased only slightly and transiently, and pregnancy continued. Finally, exogenous progesterone replacement after early luteectomy prevented otherwise inevitable miscarriage.”

Millie shook her head and smiled.

“All very complex, I see, Gerald. I’m glad I have you to help with this project. Without it, I could never do it. Not alone.”

“It’s been interesting to me as well. Given me a chance to review things I learned in vet school. Let’s go see how Tika is faring this morning.”

When they had finished their walk through the Animal Care Unit and checking on Tika, Millie and Siscom returned to Millie’s small workspace where she poured each of them a cup of coffee. Sitting across the table from Siscom, she sipped the hot liquid. Finally, she asked a question. “What are you thinking, Gerald? You looked deep in thought.”

“I was just wondering about something you said a few weeks ago before we started this venture.”

“Yeah, what’s that?”

Gerald set his cup on the table. “You mentioned that the Yeti and modern humans were somehow related in their evolutionary development, but you never mentioned the specifics. Care to elaborate?”

Millie nodded and thought for a moment. Sorting out how she was going to answer.

“Humans have twenty-three chromosome pairs in each of their cells. Chimpanzees, gorillas, and orangutans, by contrast, have twenty-four chromosome pairs. So if we are distantly related, evolution needs to explain: How did we end up with one fewer chromosome pair than them?

“As it turns out, modern genetic science has provided the answer. We need to look closely at chromosome two. In chimpanzees, gorillas, and orangutans, chromosome two is actually made up of two smaller chromosomes, two p and two q. But in humans, there is just one.

“The reason for this is the ancestral equivalents of chromosomes two p and two q fused together over the course of evolution and became the single human chromosome two.”

“How do we know that this fusion occurred?” Siscom said.

Millie smiled. “The proof is written, indelibly, in the genetic material itself. Chromosomes have different regions, including two telomeres, structures at the end of each chromosome that contain repetitive DNA and serve as a protective cap, and one centromere, a region that binds together chromosome pairs during cell division. So if the ancestral equivalents of chromosomes two p and two q fused together, end to end, to become human chromosome two, then there should be genetic proof of this evolutionary event. More specifically, that chromosome should be a bit odd--it should have telomere DNA in its middle as well as on its ends, and two centromeres, or at least, their genetic remnants, rather than one.”

Siscom leaned forward, obviously intrigued by Millie’s story. “So does human chromosome two have the telltale DNA evidence of a fusion event?” He waited pensively for her to continue the dialogue.

“Yes, it does,” Millie said. “The authors of the original 1982 Science paper had no hesitancy in declaring that the telomeric fusion of chromosomes two p and two q accounts for the reduction of the twenty-four pairs of chromosomes of the great apes to twenty-three in modern man. But they could not confirm this with the high-powered techniques of modern genetics. However, two decades later, in a study published in Nature, the precise fusion site was located on human chromosome two. The paper noted the presence of multiple subtelomeric duplications in this location, as in the expected telomere DNA, and also the vestiges of a second centromere on the chromosome that has since been inactivated. In other words--”

“In other words,” Siscom interrupted, “the genetic evidence is precisely what you would expect to see if evolution is true.”

“Yes, exactly,” Millie said. “Gerald, you understand perfectly. And that speaks volumes about the power of the theory to explain what we actually observe in the natural world.”

“It makes perfect sense when you think about it,” the veterinarian said, seemingly proud of himself.

Millie felt warmed by Siscom’s genuine interest and honored by his quick understanding of a complex idea. She was beginning to feel something more than mere professional friendship with the man. Something more personal. Her breath quickened as she continued.

“As a famous biologist said, ‘Evolution makes testable predictions. When it comes to chromosomes, the prediction of evolution is that if we have forty-six chromosomes and our closest cousins have forty-eight, then somewhere in our genome should be a chromosome formed by a recent fusion, and that chromosome should have telomere DNA, and it should have two centromeres.’ That is a prediction made by evolution, and bingo, you look, and there it is.”

“Wow,” Siscom said. “Quite a story. Any others?”

“Yes, and not nearly so involved. A retrovirus is a virus that is composed not of DNA but of RNA. Retroviruses have an enzyme, called reverse transcriptase, which gives them the unique property of transcribing their RNA into DNA after entering a cell. The retroviral DNA can then integrate into the chromosomal DNA of the host cell, to be expressed there. HIV is a retrovirus. This is a unique mechanism in the retrovirus. But it gets even more interesting. The viral DNA gets inserted into the host organism DNA. The cell then uses the viral DNA as a template for viral proteins. Instead of being co-opted, producing new viruses, and then dying, the cell lives it’s full life making new viral bodies along with everything else it’s supposed to do. This how an HIV infection works.

“If the virus attacks a gamete, then that viral genome can appear in every cell in the offspring’s body and be passed on to future generations. It sounds like a great deal for the virus. However, the viruses are very sensitive. Viral genomes are often very tight, very compact, and very susceptible to mutation. Humans and other plants and animals and other species as well have multiple copies of each gene.

“So, if one of those alleles is broken by mutation, there is a spare. Viruses and bacteria don’t have this feature. A mutation that damages the virus’s ability to perform any of the functions it must perform, such as invade a host cell, reverse transcribe the RNA, build the protein coat, means that the virus is no longer effective. The entire genome is broken, the virus can no longer function, but the DNA is still there, in the host organism. That is called an endogenous retrovirus or ERV for short.”

“But,” Siscom said, “how can this be evidence for evolution?”

Millie smiled. She was having fun explaining this to her colleague.

“Good question. Let’s say an organism gets one of these ERVs in its gametes and passes that gene onto its offspring. Except the offspring ends up with a mutation that breaks the viral gene. Now, that organism has a gene that doesn’t affect anything, but it’s there. All of that organism’s offspring will have a copy of that gene and, more telling, that gene will be in the same relative place. As time goes on and the species diverges, speciation events occur, and mutations happen, a pattern will emerge. That pattern is the same as what is predicted for the idea of common descent. That is, organisms will share a common ancestor, and those organisms that are more closely related will have a more recent common ancestor.

“A recent study of primates shows this very well. All monkeys contain two particular ERVs. All monkeys except new world monkeys share another two ERVs. Three more are shared only by gibbons, orangutans. Another two are only shared between chimps, gorillas, and humans. And three more appear only in humans. This is but a tiny bit of the thirty thousand plus ERVs in our genome. A similar situation appears in cats. If common descent were not correct, then we would not expect to see dozens of species with the exact same viral remnant in the exact same genomic position. For example, it would be highly unlikely to find a cat with the same two ERVs shared by humans, chimps, and gorillas.

“If common descent were not correct, then we would not see a relationship between shared ERVs and the closeness of two species. The more closely related the organisms, the more ERVs they share.”

“You certainly know this stuff, Millie. So the Yeti and modern humans share identical ERVs?”

“Absolutely. And none of the shared ones are shared with Neanderthals. That is how we know the Yeti diverged later than them.”

Siscom sat back and relaxed, and the two were silent for a long moment. Millie contemplated this man across from her. The depths of his ability to quickly understand complex scientific ideas amazed her. And he had a soft, quiet, unassuming nature as well. One that she found charming and engaging.

It was a thought quite new to her.