The interesting scientific question is, however; how does this particular “urge” Law work (science), given a materialistic universe (random or not).
Those organisms that don't readily reproduce, tend to not leave offspring. Those that do, tend to leave offspring. Go figure.
Imagine that, “reproductive urge” universally common within ALL life somwhere within the very framework of EVERY living organism on Earth.
Not all. Just the ones that leave offspring behind to continue the line. In every population, there are those that don't. But of course, they usually don't leave offspring.
What’s not quite understandable to my pea brain, is how peas have an “urge” (a desire or impulse) to do anything much less an urge to reproduce given a materialistic theory of evolutionary life.
Plants tend to put resources into reproduction at the expense of everything else. Why is this? Because plants that did not, tended to leave fewer offspring, often having none at all.
In a pea (or even archaea) , where exactly does this desire/impluse reside???
In the same place that your heart's urge to contract rhythmically resides.
I’m unaware of your logic or scientific observations that would support your premise/hypothesis above
.
That's how I know you don't know much about biology. It's really not all that complex in outline, although the details get pretty involved.
I’ll just simply note in passing that it’s the evolutionists (Darwin was my first example and wiki my 2018 example) that are having a problem defining an evolutionary consistent definition for “species”.
Nope. it's everyone. Darwin pointed out why. If creationism was true, species would be easy to define. But because new species evolve and because it's ordinarily a gradual process, we have lots of in-between cases. This is a very difficult problem for creationists, but it's a prediction of evolutionary theory.
That is, that fits within a consistent evolutionary framework.
Yep. It does. But as you now realize, it's completely incompatible with creationism.
To me, redbirds and blackbirds are both ...well...birds.
Just as vertebrates and bacteria are both ...well... living things. As you learned, in the strictest sense, all living things on Earth are of one kind.
Or heck, let’s just change the definition of a scientific theory to that of a scientific “fact”.
Perhaps you don't know what a theory is. What do you think it is?
Barbarian observes:
As you learned, all mutations are random. Luria and Delbruck got a Nobel for showing that adaptive mutations are random, and not in response to a need.
If I were stuck in 1943, I’d be sucking milk and pooping diapers.
Perhaps, but adaptive mutations remain random. Would you like to learn how we know?
But here’s a quick few of questions for you to ponder (I already know their answers):
1. What is gene mutation???
Technically, it's just "mutation." And there are many different kinds. Could be a point mutation, a change in a single amino acid in a protein sequence. Or it could be a chromosome duplication, fusion or fission. Or it could be an insertion of a gene into a sequence.
2. When did scientists (and engineers) develop the tools necessary to sequence the genes of an organism???
Around 1970. Actual complete sequencing of an entire genome came later.
3. When did Luria and Delbruck die???
They died at different times. Sorry.
4. If Luria and Delbruck had no way to know the sequence of bacteria genes, how did they know the bacteria’s mutations were random?
Because they were able to show that mutations such as resistance to bacteriophages, appeared even when there were no bacteriophage in the environment. The mutations just showed up randomly, whether or not there was a need for them. Would you like to learn how they discovered this?
Oh my. In your decades of studying biology, have you ever seen a scientist report that his/her experimental results has conclusively demonstrated “fact”?
Yes. Normally, scientists are very cautious and don't use the word, but it does appear in the literature as findings.
J Cell Physiol. 2018 Aug 5. doi: 10.1002/jcp.26956. [Epub ahead of print]
Cellular senescence: Molecular mechanisms and pathogenicity.
Wei W1,2, Ji S1.
Author information
Abstract
Cellular senescence is the arrest of normal cell division. Oncogenic genes and oxidative stress, which cause genomic DNA damage and generation of reactive oxygen species, lead to cellular senescence. The senescence-associated secretory phenotype is a distinct feature of senescence. Senescence is normally involved in the embryonic development. Senescent cells can communicate with immune cells to invoke an immune response. Senescence emerges during the aging process in several tissues and organs. In fact, increasing evidence shows that cellular senescence is implicated in aging-related diseases, such as nonalcoholic fatty liver disease, obesity and diabetes, pulmonary hypertension, and tumorigenesis.
Apparently, not very many. I got
214,812 hits for assertions of fact in scientific papers on the first try.
BTW, the real situation is that Luria and Delbruck’s reported a mutation rate equation (what you call fact) and it’s been updated (changed) since then.
Their finding wasn't about rates of mutation. It was that favorable mutations appear randomly and not in response to need.
MUTATIONS OF BACTERIA FROM VIRUS SENSITIVITY TO VIRUS RESISTANCE’-’
S.E. LURIAS AND M. DELBROCK
Genetics. 28 (6): 491–511
SUMMARY
The distribution of the numbers of virus resistant bacteria in series of similar cultures of a virus-sensitive strain has been analyzed theoretically on the basis of two current hypotheses concerning the origin of the resistant bacteria.
The distribution has been studied experimentally and has been found to conform with the conclusions drawn from the hypothesis that the resistant bacteria arise by mutations of sensitive cells independently of the action of virus.
The report I linked earlier shows otherwise.
Too bad for them, then. As you now see, Luria and Delbruck got their Nobel for showing that favorable mutations appear randomly.