He admitted that no one can observe macroevolution occur (in this case, a light-sensitive spot evolving eventually into a human eye). He also offered numerous links to evidence of microevolution (minor changes within species) and lateral speciation (changes in an organism that result in it being unable to reproduce with its cousins, but still being the same kind of animal).
Following is some of that proof showing "exactly . . . how" macroevolution (vertical speciation) has no empirical support.
Admissions of no evidence for macroevolution occurring, ridiculous leaps in logic, and mistaking correlation for causation, from here:
In summary, there is no barrier to species forming. This may not be enough to show that large-scale macroevolution occurs . . . For if there is enough change to form new species, and each species is slightly different from its ancestor, then simple addition shows that many speciation events can cause large-scale evolution over enough time . . . .From here:
We can test a particular claim of macroevolution. We can test, for example, if weasels are more closely related to red pandas than bears are (Flynn and Nedbal 1998, Flynn et al. 2000). This is a test of a particular evolutionary tree or scenario. It tests a historical reconstruction. If shown, on the basis of the evidence and the best data, to be wrong, then that history has indeed been falsified. But can we test the idea of common descent? It is not possible to show that something never occurred, but it is very easy to show that where it ought to occur, it either has or it hasn't. Science will not retain a bad idea when it is shown repeatedly not to explain what we have a right to expect it to explain (this is one reason why creationism was dropped from science back in the 1850s). If macroevolution persistently were shown to run counter to the data, then science would drop it and look for another solution.
Moreover, science has to an extent falsified the initial conception of macroevolution. The original idea was that evolution formed only tree-like patterns – species split like branches. A growing consensus has argued that both hybridisation (species recombining) and lateral genetic transfer (genes crossing the taxonomic boundaries individually or as part of symbiotic organisms that are taken into the "host" taxon's cellular machinery) are more common than we had previously thought. Macroevolution of species is still regarded as the most common way that the diversity of life has developed, but the "tree" now has "vines" that hang across the branches of single celled organisms (Fig. 4).
The researchers conclude that the presence of the full three-component signaling system may have played a role in the development of metazoan organisms whose cells could communicate with each other in complex ways.From here:
"It shows how evolution might work," says Wendell Lim, a researcher at the University of California, San Francisco, who was one of the authors of the paper. "Probably there was an ancestor to these organisms that first developed these chemicals."
Nothing—not even the Plague—has posed a more persistent threat to humanity than viral diseases: yellow fever, measles, and smallpox have been causing epidemics for thousands of years. At the end of the First World War, fifty million people died of the Spanish flu; smallpox may have killed half a billion during the twentieth century alone. Those viruses were highly infectious, yet their impact was limited by their ferocity: a virus may destroy an entire culture, but if we die it dies, too. As a result, not even smallpox possessed the evolutionary power to influence humans as a species—to alter our genetic structure. That would require an organism to insinuate itself into the critical cells we need in order to reproduce: our germ cells. Only retroviruses, which reverse the usual flow of genetic code from DNA to RNA, are capable of that. A retrovirus stores its genetic information in a single-stranded molecule of RNA, instead of the more common double-stranded DNA. When it infects a cell, the virus deploys a special enzyme, called reverse transcriptase, that enables it to copy itself and then paste its own genes into the new cell’s DNA. It then becomes part of that cell forever; when the cell divides, the virus goes with it. Scientists have long suspected that if a retrovirus happens to infect a human sperm cell or egg, which is rare, and if that embryo survives—which is rarer still—the retrovirus could take its place in the blueprint of our species, passed from mother to child, and from one generation to the next, much like a gene for eye color or asthma.From here, a short video purported to show "exactly . . . how" the eye evolved from a light-sensitive spot into a human eye, but in actuality offering only a chart showing a progression in the complexity of various organism's eyes and a bit of "ontogeny recapitulates phylogeny," a discredited evolutionary propaganda piece.
When the sequence of the human genome was fully mapped, in 2003, researchers also discovered something they had not anticipated: our bodies are littered with the shards of such retroviruses, fragments of the chemical code from which all genetic material is made. It takes less than two per cent of our genome to create all the proteins necessary for us to live. Eight per cent, however, is composed of broken and disabled retroviruses, which, millions of years ago, managed to embed themselves in the DNA of our ancestors. They are called endogenous retroviruses, because once they infect the DNA of a species they become part of that species. One by one, though, after molecular battles that raged for thousands of generations, they have been defeated by evolution. Like dinosaur bones, these viral fragments are fossils. Instead of having been buried in sand, they reside within each of us, carrying a record that goes back millions of years. Because they no longer seem to serve a purpose or cause harm, these remnants have often been referred to as “junk DNA.” Many still manage to generate proteins, but scientists have never found one that functions properly in humans or that could make us sick.
Then, last year, Thierry Heidmann brought one back to life. Combining the tools of genomics, virology, and evolutionary biology, he and his colleagues took a virus that had been extinct for hundreds of thousands of years, figured out how the broken parts were originally aligned, and then pieced them together. After resurrecting the virus, the team placed it in human cells and found that their creation did indeed insert itself into the DNA of those cells. They also mixed the virus with cells taken from hamsters and cats. It quickly infected them all, offering the first evidence that the broken parts could once again be made infectious. The experiment could provide vital clues about how viruses like H.I.V. work. Inevitably, though, it also conjures images of Frankenstein’s monster and Jurassic Park.
Also offered was Lenski's experiments with E. coli. Though noteworthy for showing over twenty years that the bacteria developed the ability to consume citrate without the help of plasmids, it was still just E. coli, not a newer, more complex eukaryote.