The Innsmouth Heritage and Other Sequels Read Online Free PDF

second year, and it became even more obvious that whatever I discovered wasn’t going to be of any practical import to the people whose DNA I was looking at. In a way, it didn’t matter that much to the program—the DNA that Gideon and all the rest had provided still existed, carefully frozen and stored away. The project was still healthy, still making headway.
In the third year, I finally found what I was looking for: an inversion on the seventh chromosome, which had trapped seven genes, including three oddballs. In homozygotes like Gideon, the genes paired up and were expressed in the normal way; in heterozygotes, like most of my sample—including all of the survivors—the chromosomes could only pair up if one of them became looped around, stopping several of the genes from functioning. I didn’t know what all of the genes did, or how—but my biochemical analyses had given me a partial answer.
I drove to Innsmouth the next day, in order to tell Ann the news. Although our relationship had soured and fallen apart, I still owed her as much of an explanation as I could now give.
“Do you know what Haeckel’s law is?” I asked her, while we walked beside the Manuxet, past the place where the Marsh refinery had once been located.
“Sure,” she said. “I read up on the whole thing, you know, after we got involved. Haeckel’s law says that ontogeny recapitulates phylogeny—that the embryo, in developing, goes through a series of stages which preserve a kind of memory of the evolutionary history of an organism. It’s been discredited, except as a very loose metaphor. I always thought that the Innsmouth look might turn out to have something to do with the fact that the human embryo goes through a stage where it develops gills.”
“Only the ghosts of gills,” I told her. “You see, the same embryonic structures that produce gills in fish produce different structures in other organisms; it’s called homology. Conventional thinking, muddied by the fact that we don’t really understand the business of blueprinting for physical structure, supposes that when natural selection works to alter a structure into its homologue—as when the fins of certain fish were modified by degrees into the legs of amphibians, for instance, or the forelimbs of certain lizards became the wings of birds—the blueprint genes for the new structure replace the blueprint genes for the old. But that’s not the only way it could happen. It may be that the new genes arise at different loci from the old ones, and that the old ones are simply switched off. Because they aren’t expressed any more in mature organisms they’re no longer subject to eliminative natural selection, so they aren’t lost, and even though they’re bound to be corrupted by the accumulation of random mutations—which similarly aren’t subject to elimination by natural selection—they remain within the bodies of descendant species for millions of years. If so, they may sometimes be expressed, if there’s a genetic accident of some kind that prevents their being switched off in a particular organism.”
She thought about it for a few moments, and then she said: “What you’re saying is that human beings—and, for that matter, all mammals, reptiles and amphibians—may be carrying around some of the blueprint genes for making fish. These are normally dormant—untroublesome passengers in the body—but under certain circumstances, the switching mechanism fails and they begin to make the body they’re in fishy .”
“That’s right,” I said. “And that’s what I shall propose as the cause of the Innsmouth syndrome. Sometimes, as with Gideon, it can happen very early in life, even before birth. In other instances it’s delayed until maturity, perhaps because the incipient mutations are suppressed by the immune system, until the time when ageing sets in and the system begins to weaken.”
I had to wait a little while for her next question, though I knew what it