My answer to number 1:

IC misconstrues how evolution works and assembles structures.  The recombination of genetic material can extend far above the level of single proteins or domains. Indeed, enormous chunks of genetic material may be recombined. Hence, when examining homologies, we can examine relationships that go up to the quaternary level, caused by large order duplications or recombination. Indeed, we are often tempted to think of evolutionary increment as “adding parts” or something of that like. This is a very primitive design-style worldview of looking at evolution. Indeed, the process can add parts and delete parts via these mechanisms, but this is a rare occurrence (begging the question of what a single “part” is anyway). Many complex biomolecular structures can generated by the recombination of pre-existing structures into a new role, which is a rapid-order mutation, instead of incrementation to generate the whole structure in question, incrementing generates some of the underlying mechanisms of the structure in question, and then these underlying protein structures may recombine to rapidly form the product structure. If only two or three pre-existing major components are required to generate the new and supposedly “irreducible” function, then it can be generated by what is called exaptation which is, as described, a process by which major structures (which may have no relevance per se to the function which they recombine to form) recombine and create something, which, when broken down into its fundamental constituents, appears irreducible. However, this misses the big picture of how evolution works and how functions often coalesce to form new ones by recombination, since this is generated in one or two steps, selective pressure all the way is still achieved. Now, this is true of many structures and functions, such as blood clotting (the whole chain is homologous and formed by serine duplication) or the flagellar motor (all homologous proteins, but comprised of the recombination not of individual proteins, but rather pre-existing structures, such as, in this case, the Type III secretor system of bacterial toxin pumping).

Hence, we may conclude, that instead of this backward examination (what is the effect on X if we remove a part?), which presupposes an eschatological nature of evolution whereby the system works "towards" this goal by means of "adding parts", we view evolution, not being escathological, as using exaptation to recombine pre-existing functions to create the new mechanism, in this case blood clotting. When we subdivide this not by its functional homologous relationship to other mechanisms, but rather by an arbitrary definition of a "part" is where the fallacy occurs, and the illusion of Irreducibility is generated.

More here:

 http://www.rationalresponders.com/blood_clotting_and_evolution_a_critique_of_one_of_behes_four_arguments_of_irreducible_complexity

My answer to 2:

 Whilst we used to think that the evolution of multicellular Eukaryota was essentially an expanded version of prokaryotic incremental evolution by means of the alteration of modular domains via incremental mutation mechanisms, we now know this is not the case, because of the inverse relationship between diversity and morphological complexity, thence, it is the modular alteration of Hox genes to produce modular structures whose homologous relationships are distinct across all of multiceullar Eukaryotic life, such is called convergent evolution, and the nature of homeodomains allows for rapid divergence and arisal of multicellular Eukaryota, of course, the Cambrian does not pertain specifically to the arisal of Eukaryotic multicellular organisms, since plants had already long since been in place, but rather to animals on a large scale, the rapid arisal of which is ultimately attributed to the rapid order changes by the arisal of specific Hox genes asociated with the morphological structure of animals, which of course, has modularity tracing back to before the explosion itself, anyway. The nature of Hox genes lends itself to rapid order phenotypical change as opposed to incremental selection processes, because they underlie the mechanisms . Of course, they are not the only mechanisms associated with the development of multicellular Eukaryota, we must also consider packaging, such as histone octamers, the ration of hetero/euchromatin and thence Position variegation, and methylation, genetic switches, oscillations, regulatory node pathways, etc. But the Hox genes are the most critical mechanisms for the development of any multiceullar Eukaryota because they are homeodomains and alterations in their modularity produces large scale biological structures, since multicellular Eukaryota are totally modular, and since the mitotic mechanisms are already in place, Hox genes are the mechanisms arraying the pattern by which eukaryotic cells are arranged in multicellular organisms.

This, in effect, is how we explain the arisal of large scale biological structures.

For example, on my desk I have the 29 September 2006 issue of Science, examining the following article:

Genomic Evolution of Hox Clusters: The Expression of Morphological Functions in Metazoans^[1]

In which the researchers derived orthologous relationships from the developmental along the long axis in utero of Deuterosomes, Ecdysozoans, Lophotrochozoans, and primordial bilaterial organisms from a common ancestor by their Hox genes, and comparing them to the oldest ancestral organism in possession of all the aformentioned Hox families, the Drosophila, whose embryonic development is known better than any organism except maybe the C elegans. The researchers took a confocal image of the septuple part embryonic development arrayed by the homologous relationship with the other classes by the time/divergence formula, where the relationships were derived in the following ways:

Deformed mutant stain

Sex combinations reduced stain

Antennapedia stain

Ultrabithorax stain

Abdominal-A and B stains

From this, the researchers constructed a cladogram,

From this, the reseraches constructed a developmental plant of Drosophila by the miR HOX control systems (derived mostly from the Abd-A and B stains, the Ubx stain, to construct a genetic cladogram and development plan of the diverged line, so the researchers were able to determine the precise evolutionary events shaping the Hox genes leading to the modern Drosophila. ^[2]

This same technique was applied in the next article, where researchers managed to recreate very precisely the mechanism by which the heart evolved from Cindieria, to Nematodes, Cephelolchordates, Fish, and Amniotes, by examining the expression of gene networks governing the cardiovascular sytem (NK2, MEF2, FATA, the Tbx HOX, and Hand, the genes controlling the contractile proteins which determine the fate of musculature cells in cardiological structures, and the orthologous relationship between the genes in each of the associated diverged families, and the common ancestor to which each of the proteins can be traced^[3]

In this way, the researchers built a development plan and cladogram of an impressive array of organisms and structures using the same underlying techniques, which are very effective and make extremely accurate predictions. Nothing of what you describe is present in any of the evolutionary biology articles I have ever read, since genes are studied before the gross anatomy of the organisms usually anyway, not vice versa.

 Now, the Hox Switch hypothesis was just a hypothesis untl quite recently, and although my studies into it made me believe it was a likely solution, I was not validated until several months ago, by a group of evolutionary biologists in Croata.

The only direct method of research in evolutionary history involves analysing the fossil remains of once living organisms, excavated in various localities throughout of the world.

However, that approach often cannot provide the full evolutionary pathway of some species, as it requires uncovering of many fossils from various stages of its evolutionary history. As the fossil record is imperfect, the evolution research fundamentally hinges on luck factor in discovering the adequate palaeontological sites. However, the RBI team proposed a novel and interesting approach to bypass this obstacle. Namely, they suggested that the genome of every extant species carries the ‘snapshots’ of evolutionary epochs that species went trough. What’s even more important, they also developed the method which enables evolution researchers to readily convert those individual ‘snapshots’ into the full-length ‘evolutionary movie’ of a species.

Applying their new methodology on the fruit fly genomic data they tackled some of the most intriguing evolutionary puzzles — some of which distressed even Darwin himself. First, they demonstrated that parts of the living organism exposed to the environment — so called ‘ectoderm’ — are more prone to evolutionary changes. Further, they explained the evolutionary origin of the ‘germ layers,’ the primary tissue forms that form during the first days after the conception of a new animal, and from which subsequently all other tissues are developed. Finally, they discovered the potential genetic trigger for the ‘Cambrian explosion,’ a major global evolutionary event on the planet, when some 540 million years ago almost all animal forms known today suddenly ‘appeared.’

The first public lecture on these findings was given by Dr Domazet-Loso on 4 September at 5. ISABS Conference in Forensic Genetics and Molecular Anthropology, held in Split, Croatia. The groundbreaking paper fully presenting the theory of genomic phylostratigraphy will appear in the November issue of ‘Trends in genetics,’ the most established monthly journal in Genetics.

^[1]D. Lemons and W. McGinnis, Genomic Evolution of Hox Genes Clusters,

^[2] B Alberts, Molecular Biology of the Cell, Fourth Edition, pp 454-460

^[3] E.N Olsen, Gene Regulatory Networks in the Evolution and Development of the Heart

Whilst I sympathize with this position, it is hardly an argument. There happens to be a very good reason to believe in junk DNA, it is necessary due to the nature of Eukaryotes. We must be careful not to define junk as "that which does not code for anything" as that includes obviously critical mechanisms like retrotransposons and introns and such. The relationship between base-pair baggage and phenotypic complexity is anything but linear. The Homo Sapiens has 3 billion base pairs in its genome. The amoeba has two-thirds of a trillion, 670 billion. The fish Fugu rubripes has 4 billion base pairs while the phenotypically identical pufferfish has 400 million.

Multicellular Eukaryota, being much bigger and much more complex than Prokaryota, are actually much less diverse. There are vastly more fundamental constraints and requisites on physiology, cell dynamics and anatomy in a multicellular organism than in a single-celled one. As a result, Prokaryota are vastly more diverse than multicellular Eukaryota, and are also much more diverse than Single-celled eukaryote (since Eukaryota are much more complex than prokaryota, and single-celled Eukaryota, in turn, are much more diverse than multicellular Eukaryota). This is evident if we examine the base-pair span relationship in different domains of life:

The genome is complex and intricate, but in Eukaryota, the way it is organized is just awful. It is in an alarming state of disarray. Exon chunks are strewn all over the place sandwiched between enormous and mostly useless strings of introns. What is the reason for this alarming lack of genetic housekeeping in Eukaryota? Simple, the common descent means that Eukaryota have not shed their excess baggage. They simply retain useless genetic information like a mass of old papers since it would take more energy to shed it than it would to simply retain it. Hence, Eukaryota simply retain much of their evolutionary "junk DNA" as dormant, nonexpressed strings of nucleotides which don't actually do anything, except, of course, help molecular biologists sort through evolutionary relationships. As evolution goes on, of course, this extra DNA just piles up, for there is no need for Eukaryota to shed it. This is clear indication of common descent of Eukaryota. Indeed, in humans, only 9% of our genome appears to have any function whatsoever, and thus far it has been confirmed that at least half of it is "safe for recombinative excision", which simply means that the deletion of it makes no change in the organism.

This contrasts prokaryota, which are small and energy efficient organisms for which small genomes are clearly advantageous. The result is that they have a much higher exon concentration and much less regulatory DNA (little regulatory DNA is required for a functional organism). The result is that they are much more genetically distinct and diverse than are Eukaryota.

Just stopping by to bump this thread.

And to point out that DG's post is irreducibly complex.