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I'm tempted to stop reading at his point. Anyone who thinks something can be "more impossible" than anything else doesn't have a solid grasp of language. So I'm not hopeful for where this post is going....
Turns out I was right. Another creationist who doesn't understand the difference between evolution and abiogenesis.
but its just variation. if you want to call it evolution fine. but remember that under that definition even if the bible is true evolution is true.
and when a population becomes two populations, those two populations will continue to just be variations of the same kind within their population as generations go on, gradually becoming so different to the other population as to become separate species, then on to separate families, then onto separate clades, etc.
Citation please... Where did you see this in what lab, and how has it not become mainstream news?
-_- considering the fact that we can actually sequence genomes, I'd say yes. Heck, given that species of animals is partly determined by ability to reproduce, it entirely neglects the population of Triops I am working with, which reproduce via self-fertilization. Phenotype is not the best indication of the degree of difference in genotype, however, so I wouldn't consider phenotype in and of itself to be
Actually, from looking at taxonomy so much, I'd say genus is more a measure of the number of divergences that retain certain common traits we chose to focus on rather than a consistent measure of a specific degree of similarity/difference. For example, while all members of the genus Nepenthes seem to be capable of reproducing with each other, this is not the case with all members of the genus Drosera. These are both plant genera. Genus doesn't even have consistency on whether or not the members share the same number of chromosomes.
-_- they are directly related. Rather, all changes in phenotype are not due to changes in the genome exclusively. But straight up, unless the mutation itself is neutral (like changing a codon to another codon that selects for the same amino acid), chances are the mutation will have some impact on phenotype. Assuming the cells actually use that gene to begin with, which is why mutations as an embryo cause so much more change than the mutations your cells acquire throughout adult life.
-_- note the list of regulatory genes in your source and that all of them are just as prone to being influenced by mutations as any other gene. Heck, cell specialization in and of itself is the result in only certain genes being expressed within the cell, but the process by which the excess genes are kept inactive is mediated by protein products of genes. Genes influenced by hormones and other signals given off by cells in close proximity. However, the process by which the cells do it is nevertheless a part of the genome just as much subject to mutation as anything else.
-_- your source is over a decade old and incorrectly suggests that mutation rates in microbes (which I assume to be any single celled organisms, but most likely refer to prokaryotes) are higher than in human cells: "Point mutation rates vary between organisms, and values range up to about 10^4 per base pair per generation for certain RNA viruses, around 10^6 to 10^8 for most microbes, and 10^9 per base pair per cellular generation for human cells."
How so? Very different gene combinations can result in extremely similar phenotype, so I see no reason I would need to rely on that. Mutations are not purely random, though, they are just the most random aspect of evolution. Random assumes that all mutations are equally probable, and that simply is not the case. Mutations that insert a large number of bases are far less common than ones that insert only 1, and certain regions of genomes are far more prone to mutations than others. Hence why mutations in eye color are so uncommon in humans yet more than 10% of hemophilia types A and B occur in individuals with no family history of the disease whatsoever.
You seem to be assuming that there are a ton of different traits that would be equally beneficial for a given environment, and that there aren't any traits so extremely beneficial that any environment of a given type would select for it very powerfully. For example, in all aquatic environments, having a streamlined body with very little drag is a beneficial trait to have, and there aren't many body shapes which optimize it. Thus dolphins and sharks end up with very similar body shapes despite extremely different evolutionary histories. Tons of different genomes result in similar body plans, though, so the same mutations don't have to occur to end up with this result.
Apparently so. But again, you just seem to be assuming that a lot of variation is more the result of epigenetics rather than the genes themselves changing, but this is demonstrably false (for multicellular organisms in particular). If, for example, the key differences between a polar bear and a grizzly bear were epigenetic, their genomes would be a lot more similar to each other than they actually are, to the point that they could potentially be confused for each other. Plus, there is a huge variety in epigenetic tendencies between humans, but it doesn't result in much phenotype variation, and any that does result doesn't persist for more than a few generations with any consistency. Significant and stable instances of epigenetic change resulting in changes in phenotype that are adaptive to the environment are extremely rare in multicellular organisms and they aren't stable traits that can be consistently passed on.
-_- you do know that epigenetic factors mainly turn genes off and that they aren't directly accomodating changes in environment, right? That is, people addicted to tanning that have kids aren't going to improve the ability of those kids to tan due to how tanning influences epigenetic tendencies. In fact, exposing yourself to anything that makes the process of methylation more prominent, such as smoking, decreases quality of health for oneself and the next two generations following you. The only way for methylation of a gene to be beneficial is if that gene is mutated in a very specific way and you have redundant copies of it. That is, the gene is mutated and competes with the functional variants for resources to such an extent that they can't function if it is active. And epigenetic factors aren't "pre-programmed" to target those.
Jesus Christ, the single most influential man ever, taught that "No man can come to me, except the Father which hath sent me draw him: ..." (John 6:44)
tiny changes in physical traits of living things that accumulate over very long periods of time make for large changes, and diverse species of living things.
The complexity of a motor designed by a human can itself serve as evidence for the complexity of a motor in nature designed by a designer.
If it has a function of some sort? After all... Rocks covered with moss do not drive down the highway.
With two targets. Design can mean purpose or intention. On the other hand, it can also refer to a functional arrangement of components. Design in the first sense is an unfalsifiable proposition and is not directly detectable in an object or phenomenon. Design in the second sense is determinable by observation, but does not necessarily imply design in the first sense. What it boils down to in practice is that intelligent design (that is, purposeful design) is always inferred from evidence of intelligent manufacture, rather than complexity or functionality--tooling marks, use of refined or non-natural materials, etc.
The bacterial flagella motor being designed by a designer is a plausible, falsifiable theory.
-_- all the more reason those things are not comparable in the way you want them to be.
