To reply to both points as they are the same I have combined both pieces.
Mutation are still random. There is evidence of mutagenic regulator functions in the form of reactions to stress. However this does not change the fact that mutations that occur are still random. There is no specified place in which the mutation will occur and still an incredibly low rate of success for the mutation. What the mutagenic regulators are vary from place to place where you find it and dependent on the stress but continue to be natural functions that simply interfere with the normally regulated division and reproduction processes. Even in non-stressed environments you have regular random mutations during replication. These replications can, in some cases, increase in proportion to the rest of the cells.
Alright, here's a little explanation. Here is what his link actually claims:
"What is commonly called "random mutation" does not in fact occur in a mathematically random pattern. The process of genetic mutation is extremely complex, with multiple pathways, involving more than one system. Current research suggests most spontaneous mutations occur as errors in the repair process for damaged DNA. Neither the damage nor the errors in repair have been shown to be random in where they occur, how they occur, or when they occur. Rather, the idea that mutations are random is simply a widely held assumption by non-specialists and even many teachers of biology. There is no direct evidence for it.
On the contrary, there's much evidence that genetic mutation vary in patterns. For instance it is pretty much accepted that mutation rates increase or decrease as stress on the cells increases or decreases. These variable rates of mutation include mutations induced by stress from an organism's predators and competition, and as well as increased mutations brought on by environmental and epigenetic factors. Mutations have also been shown to have a higher chance of occurring near a place in DNA where mutations have already occurred, creating mutation hotspot clusters—a non-random pattern.
While we can't say mutations are random, we can say there is a large chaotic component, just as there is in the throw of a loaded dice. But loaded dice should not be confused with randomness because over the long run—which is the time frame of evolution—the weighted bias will have noticeable consequences. So to be clear: the evidence shows that chance plays a primary role in mutations, and there would be no natural selection without chance. But it is not random chance. It is loaded chance, with multiple constraints, multi-point biases, numerous clustering effects, and skewed distributions."
https://edge.org/response-detail/25264
Let's talk about this first.
It speaks of epigenetic factors. It also points out hotspots in the genes. Also doesn't bother to mention other factors that might change someone's DNA, like a virus, for example.
Consider this. When you are born, your Mom's DNA, and your Dad's DNA combine 50/50 more or less (no one knows why by the way, the best hypothesis is because for sexual reproduction start, the costs of cells need to be same.
""This 50% cost is a
[4] The two-fold cost of sex includes this cost and the fact that any organism can only pass on 50% of its own genes to its offspring. One definite advantage of sexual reproduction is that it prevents the accumulation of genetic
mutations.
[5]""
https://en.wikipedia.org/wiki/Sexual_reproduction
They lose they same, their genes spread the same. A fair deal, if you will.) and that starts at a single cell.
During that process, their is going to be 1 or 2 mutations...
"The human mutation rate is higher in the male germ line (sperm) than the female (egg cells), but estimates of the exact rate have varied by an order of magnitude or more.
In general, the mutation rate in unicellular
eukaryotes and
bacteria is roughly 0.003 mutations per genome per
cell generation.
[4] This means that a human genome accumulates around 1-2 new mutations per generation because each full generation involves a number of cell divisions to generate gametes.
[4] The highest per base pair per generation mutation rates are found in viruses, which can have either RNA or DNA genomes. DNA viruses have mutation rates between 10−6 to 10−8 mutations per base per generation, and RNA viruses have mutation rates between 10−3 to 10−5 per base per generation.
[4] Human mitochondrial DNA has been estimated to have mutation rates of ~3× or ~2.7×10−5 per base per 20 year generation (depending on the method of estimation);
[5]"
https://en.wikipedia.org/wiki/Mutation_rate
I'll talk more about this in a second, but on with what I was saying.
So you are new human being as one cell, that replicates billions of times. Each replication, their is a chance for mutation. Genes also do not necessarily confer one outcome. One kinds of genetics happens in vitro. Meaning your mom release chemical signals to the early cells. The DNA is already prepped to receive this, and it alters how the gene expresses itself. A good example:
Left (
in vivo): Sperm and oocyte, come together at fertilization to form the totipotent zygote. After extrusion of the second polar body the maternal and paternal pronuclei (PN) migrate and fuse after several hours. Both genomes, paternal and maternal, subsequently undergo substantial epigenetic changes although at different rates. These changes are indicated for two epigenetic marks as examples to the right. Many of the central enzyme genes have been knocked out and result in a lethal phenotype. The respective phenotypes and approximate time observed are shown in the middle. Far right (
in vitro): ES cells are derived from the hypomethylated ICM and regain genome-wide DNA methylation and other epigenetic marks by the time ES cell lines are established. For most of the investigated cell types these marks appear not to change globally although locus specific changes are observed upon differentiation. As indicated by the simplified schematic of two epigenetic marks (DNA methylation and H3K27me3), many details about their presence during normal development are still lacking. The drawings are simplified and indicate global levels that remain stable. Both marks will differ between cell types in their distribution. #, lethal. ##, maintenance fine, but has differentiation defects. *
Dnmt3a knockout mice die around 3 weeks postnatally and are smaller/runted. **No observed phenotype, no observed effect on DNA methylation, effect on RNA methylation not well studied but possible. ***Mice are viable, but have hematopoietic and neural abnormalities. ****Homozygous mice are sterile, offspring of homozygous female mice and heterozygous crosses show imprinting defects and die. *****Wild-type ES cells cannot differentiate into trophectodermal cells. Loss of
Dnmt1 and global loss of DNA methylation restores this developmental potential. d.p.c., days post coitum; E, embryonic; P, paternal; M, maternal; S, sperm; O, oocyte; PN, pronuclei; EN, endoderm; ME, mesoderm; EC, ectoderm; TE, trophectoderm.
http://www.nature.com/nbt/journal/v28/n10/fig_tab/nbt.1684_F1.html
Also:
Also, your genes are coded to react to environmental conditions:
"Epigenetic phenomena in animals and plants are mediated by DNA methylation and stable chromatin modifications. There has been considerable interest in whether environmental factors modulate the establishment and maintenance of epigenetic modifications, and could thereby influence gene expression and phenotype. Chemical pollutants, dietary components, temperature changes and other external stresses can indeed have long-lasting effects on development, metabolism and health, sometimes even in subsequent generations. Although the underlying mechanisms remain largely unknown, particularly in humans, mechanistic insights are emerging from experimental model systems. These have implications for structuring future research and understanding disease and development."
http://www.nature.com/nrg/journal/v13/n2/full/nrg3142.html
Keep in mind, that evolution is premised on sexual reproduction. The mutation rate that occurs during sexual reproduction (or from replication if it's single-celled and doesn't reproduce) is the basis for evolutionary change.
The epigenetics in place to be receptive to its environment, for a codon to be expressed in more than one given determined parameters, is something that is already precoded into the DNA as a being develops from one cell to a million. Epigenetics is possible because genes are so complicated in their coding, that they already allow it,
because it beneficial to survival and reproduction. These epigenetics do not in anyway contradict in how evolution works via reproduction. In fact, they are consistent with them, and support them further, given better explanation.
Some other epigenetics, btw, include genetic damage and repair. Your gene is already coded to create proteins that, with the assistant of RNA, to repair damage in the DNA. This of course, also is genetically advantageous and increases sexual reproduction.
The damage might happen from solar damage, in which UV radiation, or living under one of the USSR's terrible, terrible nuclear testing sights, will in fact alter the DNA. In fact, it will alter the DNA of your gametes. The cells that produce the sperm. It will also damage the DNA in eggs, which are made at birth. This will result is seriously terrible reproduction.
If you ever have the stomach:
http://www.rferl.org/content/soviet_nuclear_testing_semipalatinsk_20th_anniversary/24311518.html
Also, not to mention there are thousands of viruses that are still stuck in DNA, which sometimes degrade and just stick around in the DNA for hundreds of thousands of generations...
"When scientists scan the human genome, they sometimes come across a stretch of DNA that bears the hallmarks of viruses. The easiest type of virus to recognize are retroviruses, a group that includes HIV. Retroviruses make copies of themselves by infecting cells and then using an enzyme to insert their genes into their host cell’s DNA. The cell then reads the inserted DNA and makes new molecules that assemble into new viruses.
Most of the time, retroviruses behave like other viruses, jumping from host to host. But sometimes a retrovirus will end up in the genome of an egg or sperm. If it then ends up in a new embryo, the embryo will carry a copy of the virus in every single cell–including its own egg or sperm. And on and on, from parents to children to grandchildren.
If the virus DNA remains intact, it still has the capacity to multiply. It may produce new viruses that break out of a cell, and even leap into a new host. But over the generations, the virus DNA may mutate and degrade. It may no longer be able to escape its own cell. But the virus may still have a bit of life left to it: it can make new viruses that insert their genes back into the genome at a new location. Here’s a simplified diagram of how it works…
Dewannieux and Heidmann 2013 dx.doi.org/10.1016/j.coviro.2013.08.005
This process has generated a huge amount of viral DNA in the human genome. We carry about 100,000 pieces of DNA that came from retroviruses–known as endogenous retroviruses. All told, they come to an estimated 5 to 8 percent of the entire human genome. That’s several times more DNA that makes up all 20,000 of our protein-coding genes."
http://phenomena.nationalgeographic...er-viruses-forty-million-years-in-the-making/
Alright, so let's go back to, and finish with, "random."
Earlier I sourced this:
"The highest per base pair per generation mutation rates are found in viruses, which can have either RNA or DNA genomes. DNA viruses have mutation rates between 10−6 to 10−8 mutations per base per generation, and RNA viruses have mutation rates between 10−3 to 10−5 per base per generation.
[4] Human mitochondrial DNA has been estimated to have mutation rates of ~3× or ~2.7×10−5 per base per 20 year generation (depending on the method of estimation);
[5]"
It is correct as the original article claims, that things are not "random." In actuality, they are probabilistic, or they are directly determined. The problem is, we are still on the cusp of genetics. So, what looks "random" to us at times, often has an underlying,
physical reason that we haven't figured out yet. Now that the human genome is complete, so will be proteme soon.
The ID this all speaks of by the way, a predetermined world in which the ID is not very intellgient at all. What's the "functional purpose" of having HIV implanted in your DNA? What's the "functional purpose" of UV rays from the sun, which we are always being belted with, damaging DNA to cause tumors on the body, because they altered a section of skin cells that began to grow uncontrollably? None of this has any notable goal, at least not one other than to torture humans with disease and abnormalities. Furthermore, none of it contradicts evolution by reproduction, nor does it contradict common ancestor.
"Random" is being an archaic term in genetics, because we find more physical laws that conduct things we have yet to imagine. Again, none of it implies an ID still. And none of it contradicts evolution from universal descent. It also doesn't contradict abiogenesis, etc.
So, it's all good. I hope that helps.
My point still stands true. Why does god get it wrong the overwhelming amount of time?
Your question still stands.
