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Originally posted by thehumbleone
reply to post by melatonin
Yippee.
Two
You would say melatonin, that a bird covered its eggs with some grass material and then this aided its survival when other birds around it were eaten by predators. Therefore it mated with other females and spread its genes amongst the population. However, its adaptibility to the environment would then have to be genetically transmitted to its progeny.
What some are suggesting here, is that unless parents demonstrate sex acts for their offspring... there is no way they could know how to have sex... which, of course, we know is completely ridiculous.
Proc Natl Acad Sci U S A. 1997 March 4; 94(5): 2001–2006. PMCID: PMC20032
Copyright © 1997, The National Academy of Sciences of the USA
Neurobiology
Changes in multiple brain regions underlie species differences in a complex, congenitalbehavior
Evan Balaban*
The evolutionary brain modifications that produce any complex, congenital behavioral difference between two species have never been identified. Evolutionary processes may (i) alter a single, “higher” brain area that generates and/or coordinates the diverse motor components of a complex act; (ii) separately change independent, “lower” brain areas that modulate the fine motor control of the individual components; or (iii) modify both types of areas. This study explores the brain localization of a species difference in one such behavior, the crowing of chickens (Gallus gallus domesticus) and Japanese quail (Coturnix coturnix japonica). Two major subcomponents of the behavioral difference can be independently transferred with interspecies transplantation of separate brain regions, despite the fact that these components, sound and patterned head movement, occur together in a highly integrated fashion. To our knowledge, this is the first experimental demonstration that species differences in a complex behavior are built up from separate changes to distinct cell groups in different parts of the brain and that these cell groups have independent effects on individual behavioral components.
Originally posted by Astyanax
Gosh. Lamarckism now. What next?
Permit me to add my compliments to melatonin's regarding your courage and staying power, both in this thread and more generally in the great Rearguard Action For God. Hero is a good choice of name for yourself: a tragic sort of heroism to be sure, but none the less heroic for that.
Having said which, allow me to add that if my child's biology teacher ever came out with an utterance like the one above, I'd have the sprog out of that school in a trice. Frankly, I'm shocked at such basic ignorance concerning natural selection in one of your profession.
The mutant is not the first maker of rudimentary nests - obviously - but one of its parents. The mutation takes place in one of the gametes. The first nestmaker is already genetically programmed with the new behaviour, and passes it on to its descendants through its genes, not through 'here, kids, watch Daddy and learn.'
More generally, the mutation rate in eukaryotes is in generally 10-4 to 10-6 mutations per base pair per generation[4], and for bacteria the rate is around 10-8 per base pair per generation[5]. The highest 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[5]. Human mitochondrial DNA has been estimated to have mutation rates of ~3×10-6 or ~2.7×10-5 per base per 20 year generation (depending on the method of estimation)[6]; these rates are considered to be significantly higher than rates of human genomic mutation at ~2.5×10-8 per base per generation[1].
Less obviously, perhaps, a second mutation is required. It does not have to take place at the same time; it could and probably would have occurred earlier. This mutation creates a gene for finding rudimentary nestbuilders sexy. When one of the the carriers of this gene beomes the nestbuilder's mate, the circle is closed and the stage is set for runaway sexual selection.
May I, Hero, recommend a solid, reputable popular work on sexual selection? It is The Mating Mind by Geoffrey Miller. An interesting, indeed fascinating read, not too heavy going. And he's particularly good on Fisherian runaway.
Originally posted by melatonin
Perhaps nest making was already around before birds evolved. Some birds just plop them on the ground, others make minor modifications, some dig holes, and more make more elaborate nest sites. It's just a refuge for eggs, and depending on other variables would depend the effort made.
How would a behaviour change find its way into the genome by inheritance unless it is taught.
by melatonin
Cell, Volume 121, Issue 5, 785-794, 3 June 2005
doi:10.1016/j.cell.2005.04.027
fruitless Splicing Specifies Male Courtship Behavior in Drosophila
Ebru Demir and Barry J. Dickson,
Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr. Bohr-Gasse 35, A-1030 Vienna, Austria
Summary
All animals exhibit innate behaviors that are specified during their development. Drosophila melanogaster males (but not females) perform an elaborate and innate courtship ritual directed toward females (but not males). Male courtship requires products of the fruitless (fru) gene, which is spliced differently in males and females. We have generated alleles of fru that are constitutively spliced in either the male or the female mode. We show that male splicing is essential for male courtship behavior and sexual orientation. More importantly, male splicing is also sufficient to generate male behavior in otherwise normal females. These females direct their courtship toward other females (or males engineered to produce female pheromones). The splicing of a single neuronal gene thus specifies essentially all aspects of a complex innate behavior.
Swapping a single gene between male and female swaps their courtship behaviours. Females perform male courtship behaviours to females when given the male allele.
The concept that a switch gene can specify an entire innate behaviour in no way denies the critical role of
complex gene networks, just as, for the physical building plan of an animal, the concept of a morphogenetic
switch does not deny the existence of complex regulatory networks among the genes it regulates. These
networks add both detail and robustness to the behavioural or morphological pattern initially laid down by the
switch gene at the top of the hierarchy.
Genomic and Functional Studies of Drosophila Sex Hierarchy Regulated Gene Expression in Adult Head and Nervous System Tissues
Thomas D. Goldman 1 , Michelle N. Arbeitman 1 ,2*
1 Section of Molecular and Computational Biology, Department of Biological Sciences, University of Southern California Los Angeles, Los Angeles, California, United States of America, 2 Section of Neurobiology, Department of Biological Sciences, University of Southern California Los Angeles, Los Angeles, California, United States of America
Abstract
The Drosophila sex determination hierarchy controls all aspects of somatic sexual differentiation, including sex-specific differences in adult morphology and behavior. To gain insight into the molecular-genetic specification of reproductive behaviors and physiology, we identified genes expressed in the adult head and central nervous system that are regulated downstream of sex-specific transcription factors encoded by doublesex (dsx) and fruitless (fru). We used a microarray approach and identified 54 genes regulated downstream of dsx. Furthermore, based on these expression studies we identified new modes of DSX-regulated gene expression. We also identified 90 and 26 genes regulated in the adult head and central nervous system tissues, respectively, downstream of the sex-specific transcription factors encoded by fru. In addition, we present molecular-genetic analyses of two genes identified in our studies, calphotin (cpn) and defective proboscis extension response (dpr), and begin to describe their functional roles in male behaviors. We show that dpr and dpr-expressing cells are required for the proper timing of male courtship behaviors.
It takes quite a lot of variation to make a knot
By the behaviour being genetically mediated in the first place. I think astyanax summarised it much more eloquently than I. If the genetically-mediated behaviour is open to variation, then selection can act. I'll send you back to the initial study about homology and grooming FAPs in rodents.
I think FAPs are a form of instinct by their very nature. I suppose it's not impossible for certain learned behaviours to become instinctive over time. Maybe. The problem is that you want to make a very clear distinction between instinct and learning. As noted earlier, instincts can be influenced by experience. For example, birds will develop their species specific song when raised in a sound proof area, but can still learn more complex song when eventually exposed to other bird's songs.
Originally posted by Heronumber0
So what you are saying is that a mutation occurred in the gametes to change the behaviour of the birds? Do you know what you are saying?
You are saying that a random mutation targeted a complex hierarchy of genes involved in the building of nests to change the type of nest building.
Out of all the genes available, the precise genetic mutation was created.
Do you know that even if the sequence of the genes and genomes is known, it takes up to a year of careful selection and screening to perform gene mutation in a lab.
Do you also have a knowledge of the rate of mutations? ...From a brief scan of wiki, I came up with this:
More generally, the mutation rate in eukaryotes is in generally 10-4 to 10-6 mutations per base pair per generation... these rates are considered to be significantly higher than rates of human genomic mutation at ~2.5×10-8 per base per generation[1].
The average mutation rate was estimated to be ~2.5 x 10-8 mutations per nucleotide site or 175 mutations per diploid genome per generation.
Source
What I am saying here is that it is quite unlikely that germ line (sperm or egg) mutations would target a hierarchy of nest building genes.
After this amazingly fortuitous event, the mutation would then be passed on to a 'normal' female let's say. The female's chicks would then have one mutated chromosome and one normal (or wild type) chromosome. You have created hybrid chicks which would exhibit both behaviours or a mixture of both, or neither- something called displacement behaviour.
Shall we go back a step. And please don't offer your own opinions as fact as Darwinian supporters are likely to do. The weaver bird must make one knot to a branch...
The sheer complexity of the processes that underly instinct are enormous and mind-blowing... His artistry and genius down to every protein made by every cell of every weaver bird... Natural Selection is one of God's biological Laws.
Originally posted by Heronumber0
In fact, the change in transcription of the fruitless gene affects quite a number of genes. As I said, it is likely that single gene knockout to change an FAP/instinctive behaviour is actually multigenic in its influence hence the tentative language used by the researchers from the Press release.
It takes quite a lot of variation to make a knot
I repeated my mistake here but I was referring to the appearance of an adaptive behaviour. For example, if a bird can make a more complex but greater load bearing structure then the correct genes for the adaptation have to be either:
a) selected for;
or b) passed on to the next generation.
The easiest way for the selection would have to be by an extraordinary success of predators or for the successful bird to be extraordinarily promiscuous in order for that genetic structure to be inherited. Moreover any mutation would have to be extraordinarily successful as well. But I suppose infinite Time does have its advantages...
from Atyanax
Do you know what's wrong with this sentence? One word: 'targeted'.
Teleology again. We're speaking of random occurrences here. I'll come back to that.
Many others occurred (or 'were created'). Some were deleterious, and their owners died out. Some were selectively neutral for the nonce and hung around in the population without doing much. A few of these, like the gene for finding nestbuilders sexy, ultimately ended up conferring a selective advantage in combination with a subsequent mutation. And some - a very, very few - conferred an advantage in their own right.
More generally, the mutation rate in eukaryotes is in generally 10-4 to 10-6 mutations per base pair per generation... these rates are considered to be significantly higher than rates of human genomic mutation at ~2.5×10-8 per base per generation[1].
Following the link in the footnote given above, I found
The average mutation rate was estimated to be ~2.5 x 10-8 mutations per nucleotide site or 175 mutations per diploid genome per generation.
Source
175 mutations per diploid genome. The source looks fairly kosher to me. Am I displaying my ignorance here, or isn't a eukaryotic diploid genome the full set of genes for an individual? Doesn't that mean each individual human being is a mutant 175 times over? Gosh, that's a lot of mutations. How many, then, must have taken place over the tens of thousand of generations that Homo has been Sapiens?
The human genome has, what, three billion base pairs? Sounds like there's been been time enough to mutate every single base pair on the genome.
But - since I am not a biologist - I could be totally ignorant of a hundred reasons why this cannot be so. I am willing to learn; teach me.
Sounds like plenty of time for those nestbuilding birds to mutate. All the time in the world.
Because, remember, it's random. The chance of a useful mutation is vanishingly small - but any mutation can be that mutation. It's not targeted: if someone's flinging cosmic-ray bolts, he's not taking aim and he doesn't have to. Because it doesn't matter that most mutations are pointless or harmful. What matters is there are so many.
Answered above Asty.
Why not? Everything we are, all our amazing elaboration from embryos to Heroes, is already encoded in our genes, to be unfolded in ways that are susceptible to modification by our environments. It follows that a mutation in a gamete can affect any gene or genes - and thus affect any kind of behaviour, nestbuilding included.
Correct me if I am wrong on this but I believe the condition is called heterochromia iridis and is environmental in origin:
Why can't one gene be expressed and its counterpart on the other chromosome recessive? Happens all the time. People with one blue and one brown eye aren't that common.
No, Teacher, let's not go back a step. Confound the knot and to perdition with the branch. You are trying to insist that evolution must have happened the way you say it did. Instead of thinking of how some bird could must suddenly have upped and tied a pefect knot from scratch, try to imagine how a weaverbird's nest might have evolved. It strikes me as a much more fruitful line of inquiry.
We are indeed a part of, completely permeated by, and act in the presence of something that can most fittingly be called God. By all means speak of natural selection as God's law, if it comforts you; speak also of the great universal laws, the laws of motion, of thermodynamics, of gravitation in such terms - why not? But I conceive of this God as no external agent, no uncaused Cause hiding in the wings of Creation. It is simply the Universe, what Christians call the World. Such is what you would call my blasphemy, for to you I embrace Creation and spurn the Creator. But for me - an atheist withal - Creator and Creation are one and the same.
I trust you will forgive the slight digression. You are not the only one who has thought long and hard on these matters.
by nj2day
You're letting the numbers daunt you again...
Suppose there is a 1 in a billion chance of something happening... now... repeat the experiment 100 billion times...
There's a statistical probability of this unlikely event happening 100 times out of that 100 billion...
by nj2day now suppose that 1 off chance actually produced something beneficial to the species... something that improved their odds of spreading their DNA to offspring... who now have a leg-up to thwart the forces of natural selection...
Many mutations aren't benificial for survival.... at first...
Suppose this mutation is carried on part of the DNA that isn't currently used... but, for some reason, in the future, it gets clicked into the "on" position... Now suddenly, that DNA mutation happens to be beneficial for survival..
It takes 7 very specific genetic mutations for a cell to become cancerous... that doesn't seem like very good odds to me... but... given the amount of cells in each human body, multiplied by the amount of humans running around... means that the improbability of these 7 specific mutations happening is overcome... and thus we have cancer... these mutations are VERY benificial to the cancerous cells, as it inhibits all checks and balances to keep the cell from dividing (reproducing itself), and allows it to propagate uncontrollably.
The many causes of cancer
Carcinogens
Age
Your genetic make up
Your immune system
Your diet
Your day-to-day environment
Viruses
Interesting information - I thought there were 7 stochastic events, any one of which in excess could produce cancer. However, the state of the immune system is also important. How does it cause a genetic change? And how does the wrong diet cause a specific genetic change?
Here's your link with the cancer information...
health.usnews.com...
I had another earlier that stated that on average, 7 specific genetic mutations are required to complete the genetic pathway for cancer to develope... out of the 7, two are capable of being passed down through heridity...
meaning... if you inherit the gene for cancer, you are already 2 steps ahead in accumulating these mutations than someone who didn't inherit them...
If you notice the list... they all are sort of inter-related... Diet and age effect immune system... etc... its all about accumulating these mutations...
"Rogue cells" do have a chance to get caught by the immune system before they become full on cancer/tumors... btw
Anyway, I'll keep looking for my source document that names specifically 7 mutations...
Point of interest:
They have discovered 12 different "pathways" for these mutations to result in cancer... which means, there are 12 different sets of 7 mutations.... all leading to cancer
[edit on 18-2-2009 by nj2day]
What is the cancer genome, anyway?
Cancer, by definition, is caused by genes going haywire—mutating in ways that are not part of the normal blueprint for the body's form and function. Even among tumors of a single type, those genes can go haywire in many different ways. So describing the entire cancer genome involves characterizing all the different abnormalities that are linked to each of the 50 major types of cancer. That daunting task would involve churning through 12,500 times as much information as scientists processed in their recently completed effort to map the entire human genome.