|July 21, 2012||Posted by News under Biology, News|
” … receiving 28% fewer citations overall for each additional equation per page in the main text.”
|May 5, 2012||Posted by News under Biology, News|
He wasn’t a tenured bore.
James Barham at Best Schools ‘fesses up III: Biology (like the social sciences) is guilty of massive and systematic equivocation
|March 15, 2012||Posted by News under Biology, Culture, Intelligent Design|
“Biologists are constantly basing nearly all their work on an unspoken assumption of the “usefulness” or “efficiency” or “rationality” or “intelligence” of biological systems, even if they would strenuously deny the fact. “
|February 6, 2012||Posted by News under Biology, Evolution, News|
“a 150 million years earlier than when other animals emerged in the fossil record.”
|February 5, 2012||Posted by News under Biology, Intelligent Design, News|
“I conclude that scientists, philosophers, and ethicists should discard the project of defining life.”
|January 20, 2012||Posted by kairosfocus under Biology, Design inference, Genetics, ID Foundations, Intelligent Design|
(Series on Front-loading continues, here) As we continue the ID Foundations series, it will be necessary to reflect on a fairly wide range of topics, more than any one person can cover. So, when the opportunity came up to put Front-Loading on the table from a knowledgeable advocate of it, Genomicus, I asked him if […]
|December 12, 2011||Posted by News under Biology, Darwinism, News|
Most biological students think that adaptive radiations and Darwinism go together, and that the mechanisms of genetic mutation and natural selection explain all the data. … However
|December 4, 2011||Posted by News under Biology, News|
“The top tier publications are often run by professional editors who do not work in a lab, and who do not moderate the peer-review process.”
Researchers hope butterfly genome sequence explains migration – but their approach raises a critical question
|November 29, 2011||Posted by News under Biology, Intelligent Design, News|
It will be most interesting if the mechanism indeed turns out to be fundamentally the same for butterflies, birds, and turtles. What would such a finding imply?
|November 16, 2011||Posted by News under Biology, News|
And you have never seen anything like it.
|November 15, 2011||Posted by News under Biology, News, Video|
|November 14, 2011||Posted by News under Biology, News|
You can see a brick of the shelter the rotifer builds around it, ready to be added, in the winning photo.
|November 14, 2011||Posted by News under Biology, News|
|November 12, 2011||Posted by News under Biology, Design inference, Intelligent Design, News|
From our moral and intellectual superiors, no less.
|November 2, 2011||Posted by News under Biology, Intelligent Design, News|
Plus the Ontario premiere of Metamorphosis – the film on why butterflies make nonsense of Darwinism.
Cell biology: A “spindle checkpoint” mechanism prevents cancer cells in a variety of life forms, humans to yeast
|November 2, 2011||Posted by News under Biology, Intelligent Design, News|
“Amazingly” crops up as often in cell biology these days as “groovy” used to among hippies.
|October 31, 2011||Posted by News under Biology, News|
“The algorithms organize the intertwined 3D surface-contour data into simplified orthogonal cell abstractions and the components can be sorted to emphasize particular comparisons with proximity. “
|October 10, 2011||Posted by News under Biology, Culture, News|
Preliminary application form deadline October 31, 2011
|October 8, 2011||Posted by News under Biology, Evolution, News|
From Thomas Hayden, “How to Hatch a Dinosaur” (Wired September 26, 2011): Human beings are almost indistinguishable, genetically speaking, from chimpanzees, but at that scale we’re also pretty hard to tell apart from, say, bats. Yeah, it figures. Batman. Hints of long-extinct creatures, echoes of evolution past, occasionally emerge in real life—they’re called atavisms, rare […]
|September 15, 2011||Posted by Jonathan M under 'Junk DNA', Biology, Evolution, Evolutionary biology, Genetics, Genomics, Human evolution|
Those of you who have been following this blog, as well as Evolution News & Views, for some time, will be aware that I have previously discussed, across multiple articles, the phenomenon of endogenous retroviral inserts into the genomes of primates. Those familiar with the debate over origins will also be familiar with the various […]
We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome. Humans contain an intact preintegration site at this locus. These observations provide very strong evidence that, for some fraction of the genome, chimpanzees, bonobos, and gorillas are more closely related to each other than they are to humans. [emphasis added]
Could this be evidence for a site-specific target bias rather than common ancestry?
But there’s more.
Another study, by Sverdlov (1998) reports,
But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified ‘hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically. [emphasis added]
I could continue in a similar vein for some time. Other classes of retroelement also show fairly specific target-site preferences. For example, Levy et al. (2009) report that Alu retroelements routinely preferentially insert into certain classes of already-present transposable elements, and do so with a specific orientation and at specific locations within the mobile element sequence. Moreover, a study published in Science by Li et al.(2009) found that, in the waterflea genome, introns routinely insert into the same loci, leading the internationally-acclaimed evolutionary biologist Michael Lynch to note,
Remarkably, we have found many cases of parallel intron gains at essentially the same sites in independent genotypes. This strongly argues against the common assumption that when two species share introns at the same site, it is always due to inheritance from a common ancestor.
A recent study by Spradling et al. (2011) documented Drosophila P elements preferentially transpose to replication origins. They report,
P element insertions preferentially target the promoters of a subset of genes, but why these sites are hotspots remains unknown. We show that P elements selectively target sites that in tissue-culture cells bind origin recognition complex proteins and function as replication origins.
Finally, Daniels and Deininger (1985) suggest that,
…a common mechanism exists for the insertion of many repetitive DNA families into new genomic sites. A modified mechanism for site-specific integration of primate repetitive DNA sequences is provided which requires insertion into dA-rich sequences in the genome. This model is consistent with the observed relationship between galago Type II subfamilies suggesting that they have arisen not by mere mutation but by independent integration events.
What About Shared Mutations in ERVs?
Regarding shared “mistakes” between primate genomes, this argument again assumes that mutations are random and are unlikely to occur convergently. Cuevas et al. (2002), however, have documented, in retroviruses, the occurrence of molecular convergenes in 12 variable sites in independent lineages. Some of these convergent mutations even took place in intergenic regions (changes in which are normally thought to be selectively neutral) and also in synonymous sites. The authors also note that this observation is fairly widespread among HIV-1 virus clones in humans and in SHIV strains isolated from macaques, monkeys and humans.
As the authors note,
One of the most amazing features illustrated in Figure 1 is the large amount of evolutionary convergences observed among independent lineages. Twelve of the variable sites were shared by different lineages. More surprisingly, convergences also occurred within synonymous sites and intergenic regions. Evolutionary convergences during the adaptation of viral lineages under identical artificial environmental conditions have been described previously (Bull et al. 1997; Wichman et al. 1999; Fares et al. 2001). However, this phenomenon is observed not only in the laboratory. It is also a relatively widespread observation among human immunodeficiency virus (HIV)-1 clones isolated from patients treated with different antiviral drugs; parallel changes are frequent, often following a common order of appearance (Larder et al. 1991; Boucher et al. 1992; Kellam et al. 1994; Condra et al. 1996; Martinez-Picado et al. 2000). Subsequent substitutions may confer increasing levels of drug resistance or, alternatively, may compensate for deleterious pleiotropic effects of earlier mutations (Molla et al. 1996; Martinez-Picado et al. 1999; Nijhuis et al. 1999). Also, molecular convergences have been observed between chimeric simian-human immunodeficiency viruses (strain SHIV-vpu+) isolated from pig-tailed macaques, rhesus monkeys, and humans after either chronic infections or rapid virus passage (Hofmann-Lehmann et al. 2002).
I could cite several other similar studies. For another case example, see Bull et al. (1997), which documents that,
Replicate lineages of the bacteriophage X 174 adapted to growth at high temperature on either of two hosts exhibited high rates of identical, independent substitutions. Typically, a dozen or more substitutions accumulated in the 5.4-kilobase genome during propagation. Across the entire data set of nine lineages, 119 independent substitutions occurred at 68 nucleotide sites. Over half of these substitutions, accounting for one third of the sites, were identical with substitutions in other lineages. Some convergent substitutions were specific to the host used for phage propagation, but others occurred across both hosts. Continued adaptation of an evolved phage at high temperature, but on the other host, led to additional changes that included reversions of previous substitutions. Phylogenetic reconstruction using the complete genome sequence not only failed to recover the correct evolutionary history because of these convergent changes, but the true history was rejected as being a significantly inferior fit to the data. Replicate lineages subjected to similar environmental challenges showed similar rates of substitution and similar rates of fitness improvement across corresponding times of adaptation. Substitution rates and fitness improvements were higher during the initial period of adaptation than during a later period, except when the host was changed.
What About LTR-LTR Divergence?
Darwinists sometimes argue that the degree of LTR-LTR divergence (in the context of the relative age of a given insertion) can be used as a predictive tool to demonstrate common ancestry. The argument goes that, because LTRs are thought to accumulate mutations at a roughly equivalent rate, LTRs which are highly divergent should correspond to an older integration, whilst LTRs which are less divergent should correspond to a younger insertion. The problem is that the pattern is nothing like as neat and tidy as Darwinists would like. Hughes and Coffin (2005) report that,
HERV elements make up a significant fraction of the human genome and, as interspersed repetitive elements, have the capacity to provide substrates for ectopic recombination and gene conversion events. To understand the extent to which these events occur and gain further insight into the complex evolutionary history of these elements in our genome, we undertook a phylogenetic study of the long terminal repeat sequences of 15 HERV-K(HML-2) elements in various primate species. This family of human endogenous retroviruses first entered the primate genome between 35 and 45 million years ago. Throughout primate evolution, these elements have undergone bursts of amplification. From this analysis, which is the largest-scale study of HERV sequence dynamics during primate evolution to date, we were able to detect intraelement gene conversion and recombination at five HERV-K loci. We also found evidence for replacement of an ancient element by another HERV-K provirus, apparently reflecting an occurrence of retroviral integration by homologous recombination. The high frequency of these events casts doubt on the accuracy of integration time estimates based only on divergence between retroelement LTRs. [emphasis added]
Summary & Conclusion
In summary, the stupendous claim that there is overwhelming evidence that humans and chimpanzees have common ancestry is an overstatement. The arguments for common ancestry based upon shared ERV elements needs to be considered in the context of other evidence as well (such as that from embryology), which clearly militates against the paradigm of common descent. And then there is still the lack of any feasible naturalistic evolutionary mechanism which can account for the complexity of life. When all the facts are in, I am inclined to be very skeptical of not just the claims of neo-Darwinism to be able to explain all of life, but also that the observed molecular patterns are robust evidence for the common ancestry model. If it is the case, as has been suggested by some, that these HERVs are an integral part of the functional genome, then one might expect to discover species-specific commonality and discontinuity. And this is indeed the case.