Rh gene

I'm A-, had the RhoGam shot during and after two of my pregnancies. The other two I did not get the shot after, I guess because they were negative as well. Not sure. However, I have 'dirty' blonde hair (was born a platinum blonde) and green eyes. My two kids that may be RH- have brown hair and hazel eyes. Not sure what having this RH- blood truly means other than I would die if given RH+ blood.... I am also not sure where I got RH- blood from, as both my parents are positive... Very interesting...

There are some really good threads about this same topic on ATS already.
Just search it and ye shall find.

originally posted by: Temudjin
a reply to: chr0naut

And how long does that take ?

Not quite sure what you mean?

Mutational changes arise spontaneously in individuals, they don't necessarily 'take time'.

Mutation to one or two nearly adjacent genes can happen in a single step.

In the mutation that gives rise to RH- blood, it is the absence of genes and represents genetic damage that deletes or makes inviable very few physically closely spaced genes. It is not that unlikely and you do not have to invoke evolutionary gradualism to explain it.

Also, RH disease is usually caused by the baby carrying the gene from the father. The fact that most offspring survive indicates that this isn't a speciating change.

a reply to: chr0naut

So the most common cause for genetic mutation of this sort is genetic damage and not survival? Sickle cell in africa is damaged genetics or is it evolution?
And the linear -evolution created a humanoid for the cold climate to survive in north which we see in most scandinavians. Could it be the most beneficial gens survived of the climate it lived in.

Evolution is about survival to ones surroundings, the beneficial mutations survives.

a reply to: Menrva

I can receive any blood type, cause im a AB positive, but your body would kill you if i gave my blood to you.

originally posted by: Temudjin
a reply to: chr0naut

So the most common cause for genetic mutation of this sort is genetic damage and not survival? Sickle cell in africa is damaged genetics or is it evolution?

It's not an either/or proposition though. What Chr0naut is referring to is a mutation or mutations in an individual. Evolution is measured in entire populations. What you are referring to as genetic damage may in fact be beneficial to the individual. If that individual survives and reproduces then his or her genes will propagate throughout the local population provided it is in fact beneficial to the population as a whole.

As for sickle cell, it really depends on perspective and environment. If you are in a tropical climate and you've got malaria, it's clearly a beneficial and advantageous mutation. If you aren't stricken with malaria and you have an episode and don't treat it quickly then it's a very non- beneficial mutation.

And the linear -evolution created a humanoid for the cold climate to survive in north which we see in most scandinavians. Could it be the most beneficial gens survived of the climate it lived in.

Evolution isn't linear. It's a measurement of changes in allele frequency over time across populations. It varies from one individual to the next. In regards to Scandanavians, it's not the temperature they are adapted to it's the latitude and amount of sunlight they receive in regards to production of vitamin D.

Evolution is about survival to ones surroundings, the beneficial mutations survives.

On one hand, yes this could be considered true. Neanderthal for example, were extremely well adapted to a colder European and West Asian climate. In the end that degree of specialisation was part of their downfall. They weren't able to expand into other ecological niches because they were too adapted to the cold. H. Sapient Sapiens on the other hand were able to adapt and thrive in a variety of niches. It's our ability to shape the environments t suit our needs as opposed to changing to suit the environment that led to our success as a species.

a reply to: Temudjin

Now how does it work?

Look it up.

I've seen the characteristics of mRNA and saw a mutation called Eve then much later Adam but they both didn't occur in the same time nor the same continent.

Current evidence says you may be wrong on both counts. Mitochondrial Eve and Y-chromosomal Adam have always both been placed in Africa, which is the same continent. In 2013, a previously unknown Y haplogroup (A00) was announced that moved the range of years for both mEve and yAdam to have significant overlap.

It's called the Babylon dispersion,

Can you elaborate?

are polar bears and grizzlies the same species since they could mate and give offspring in the same way a liger functions?

Most likely, yes, polar bears and grizzlies are the same species. It's more likely they should both be considered subspecies of either Ursus arctos or Ursus maritimus. This is why taxonomy is an imperfect part of biology, at best. Grizzlies and polar bears are probably about as closely related as dogs and wolves, or Canis lupus familiaris and Canis lupus lupus, respectively. All of these examples are unlike ligers, in that ligers are sterile.

Ever heard of the myth of the Giants? introgressive hybridization And back crossing? Evolution is a linear survival mechanism, I'm baiting if you are wondering what im doing.

Yes, and it's borrrrrrrrrring. Say what you're going to say, or go back to lurking for a while until you understand what ATS is and isn't for. Hint: what you're doing now is what it isn't for.

I'm saying that a more evolved species came into the homo sapien population, which has the same traits as a polar bear, you can call them whatever you want I call them Neanderthals.

Why do you assume that Homo neanderthalensis are more highly evolved than Homo sapiens? What does "more highly evolved" even mean? Further, I suspect that as we come to understand our cousins more and more, we'll start naming them differently on a taxonomic level... it'll be more like Homo sapiens sapiens, Homo sapiens neanderthalensis, Homo sapiens denisova, etc.

originally posted by: iterationzero
a reply to: Temudjin

it'll be more like Homo sapiens sapiens, Homo sapiens neanderthalensis, Homo sapiens denisova, etc.

NOw we talking!! So just to jump the gun, when you thinkwe be seing this?

a reply to: Temudjin

We already see this with some anthropologists. There is a growing minority who list them taxonomically as such.

originally posted by: peter vlar

originally posted by: Temudjin
a reply to: chr0naut

So the most common cause for genetic mutation of this sort is genetic damage and not survival? Sickle cell in africa is damaged genetics or is it evolution?

It's not an either/or proposition though. What Chr0naut is referring to is a mutation or mutations in an individual. Evolution is measured in entire populations. What you are referring to as genetic damage may in fact be beneficial to the individual. If that individual survives and reproduces then his or her genes will propagate throughout the local population provided it is in fact beneficial to the population as a whole.

...

Thanks peter vlar.

I was not talking in terms of evolutionary gradualism (which is becoming harder to justify in the light of the number of actual examples of punctuated evolution) but in individual cases of mutation.

Too many people cite gradualism as explanation, ignoring that the mutation must arise in individuals prior to its spread though the gene pool. Without the mutation, there is nothing to spread.

This is easy to explain in the case of mutation that is not a speciating one (like RH factor) but if a mutant cannot breed with its source gene pool, it is speciated and its mutation simply cannot spread by methods proposed under current theory.

Many evolutionists propose that the specation change is incremental and therefore gradualism explains how a new species may eventually arise as each slight divergence adds to the overall differences until a population can no longer breed with its ancestors.

Yet we know that on chromosone six there are about 100 biocompatibility genes (a small number and proximally close) any one of which may potentially confer sufficient incompatibility to be speciating.

Speciation can (and does) happen in a single step - a single mutation. There are many fetal immune related diseases that attest this (most survivable if the immune response of mother and child are suppressed).

The success of the mutation affecting RH factor demonstrates this, that mutational speciation does not 'fit' with evolutionary gradualism.

This does not invalidate evolution. It just shows that the current accepted system is too simplistic and missing alternate mechanism/s (in my opinion). For example, one solution might be the simultaneous mutation of several compatible speciated individuals. Say from a mutation induced by a virus or targeted toxin ('gene shears' being one such actual laboratory example).

Much of what we do when we manipulate genetics are natural processes but these natural processes are noticeably absent from evolutionary theory.

We have simple reasonable and demonstrable examples of how genetic change may occur that are just not considered in evolutionary theory!

So, we must conclude, it is incomplete.

(Gets off soapbox. Please excuse my rant but it was slightly on topic).

originally posted by: chr0naut
[
Thanks peter vlar.

I was not talking in terms of evolutionary gradualism (which is becoming harder to justify in the light of the number of actual examples of punctuated evolution) but in individual cases of mutation.

Too many people cite gradualism as explanation, ignoring that the mutation must arise in individuals prior to its spread though the gene pool. Without the mutation, there is nothing to spread.

This is easy to explain in the case of mutation that is not a speciating one (like RH factor) but if a mutant cannot breed with its source gene pool, it is speciated and its mutation simply cannot spread by methods proposed under current theory.

Can you actually site any examples that support this though? I'm not trying to bust your balls, I've been out of the Anthropology game for several years and tend to keep up with my former area of research but only poke my head into other areas if something really cool catches my eye so it's entirely likely that a piece of research has escaped my attention and if that's the case then I'm all for looking into it.

Many evolutionists propose that the specation change is incremental and therefore gradualism explains how a new species may eventually arise as each slight divergence adds to the overall differences until a population can no longer breed with its ancestors.

This is still the case with Punctuated Equilibrium. Its just that particular mutations spread much quicker through populations this way. It was also a very different scenario in the past with populations in the 10's of thousands, or even lower after the Toba event, compared to the billions of individuals we have with HSS currently. Our current population levels over the past millennia are unprecedented in hominin history.

Yet we know that on chromosone six there are about 100 biocompatibility genes (a small number and proximally close) any one of which may potentially confer sufficient incompatibility to be speciating.

Speciation can (and does) happen in a single step - a single mutation. There are many fetal immune related diseases that attest this (most survivable if the immune response of mother and child are suppressed).

Personally, I think you're being way too conservative with how you use speciation. No matter how you look at it, it is still a measure of population wide genetics. I'm an ardent supporter of Gould and Punctuated Equilibrium which was still fairly well frowned upon in the 90's when I was in school and which I took a lot of flack over. But speciation still does not occur on an individual level. Even with all of the hemolytic factors involved in Rh differential pregnancies, there is no guarantee of death of the fetus or newborn thus the breeding is successful in these individuals. Were that not the case, we would not see such widespread variation in serology. There is no absolute need for medical intervention as the hemolytic issues vary widely from extreme(where miscarriage is the result) to so mild that there is no noticeable affect on the offspring.

The success of the mutation affecting RH factor demonstrates this, that mutational speciation does not 'fit' with evolutionary gradualism.

As I describe above, I honestly don't think this is the case. It's not as if Rh factors have created a speciation event.

This does not invalidate evolution. It just shows that the current accepted system is too simplistic and missing alternate mechanism/s (in my opinion). For example, one solution might be the simultaneous mutation of several compatible speciated individuals. Say from a mutation induced by a virus or targeted toxin ('gene shears' being one such actual laboratory example).

except that if you're talking about a speciation event, then the individuals would not be compatible.

Much of what we do when we manipulate genetics are natural processes but these natural processes are noticeably absent from evolutionary theory.

Which ones? just trying to make sure I'm following you clearly here and not make an assumption.

We have simple reasonable and demonstrable examples of how genetic change may occur that are just not considered in evolutionary theory!

And they would be?

So, we must conclude, it is incomplete.

I don't know any Anthropologists or Evolutionary Biologists who would realistically disagree with that statement. One must keep in mind though that what is discussed is typically what is known for certain currently, things that can be demonstrated to be true. If there is more out there and the data supports it, current views on evolution will change just like it was contentious 20 years ago to say that Humans bred fertile offspring with Neandertal and it is currently an accepted fact.

(Gets off soapbox. Please excuse my rant but it was slightly on topic).

Rant away! An exchange of ideas is never a negative thing if either side is willing to learn something from it.

a reply to: peter vlar

a reply to: chr0naut

continue please

originally posted by: Temudjin
a reply to: peter vlar

a reply to: chr0naut

continue please

You don't have any input of your own beyond one liners in your own topic?

a reply to: Barcs

I do have my own input, however if expertise are in, i tend to read what they have to say. Its a wonderful thing

originally posted by: peter vlar

originally posted by: chr0naut
[
Thanks peter vlar.

I was not talking in terms of evolutionary gradualism (which is becoming harder to justify in the light of the number of actual examples of punctuated evolution) but in individual cases of mutation.

Too many people cite gradualism as explanation, ignoring that the mutation must arise in individuals prior to its spread though the gene pool. Without the mutation, there is nothing to spread.

This is easy to explain in the case of mutation that is not a speciating one (like RH factor) but if a mutant cannot breed with its source gene pool, it is speciated and its mutation simply cannot spread by methods proposed under current theory.

Can you actually site any examples that support this though? I'm not trying to bust your balls, I've been out of the Anthropology game for several years and tend to keep up with my former area of research but only poke my head into other areas if something really cool catches my eye so it's entirely likely that a piece of research has escaped my attention and if that's the case then I'm all for looking into it.

I am at a loss, as I cannot provide any examples of speciation that did not happen due to to the inability to breed. What evidence would there be for that? Perhaps you could provide some actually observed evidence of speciation occurring despite the speciated oganisms inability to breed, which would negate what I proposed?

Many evolutionists propose that the specation change is incremental and therefore gradualism explains how a new species may eventually arise as each slight divergence adds to the overall differences until a population can no longer breed with its ancestors.

This is still the case with Punctuated Equilibrium. Its just that particular mutations spread much quicker through populations this way. It was also a very different scenario in the past with populations in the 10's of thousands, or even lower after the Toba event, compared to the billions of individuals we have with HSS currently. Our current population levels over the past millennia are unprecedented in hominin history.

Yet we know that on chromosone six there are about 100 biocompatibility genes (a small number and proximally close) any one of which may potentially confer sufficient incompatibility to be speciating.

Speciation can (and does) happen in a single step - a single mutation. There are many fetal immune related diseases that attest this (most survivable if the immune response of mother and child are suppressed).

Personally, I think you're being way too conservative with how you use speciation. No matter how you look at it, it is still a measure of population wide genetics. I'm an ardent supporter of Gould and Punctuated Equilibrium which was still fairly well frowned upon in the 90's when I was in school and which I took a lot of flack over. But speciation still does not occur on an individual level.

It is nonsense double-think to talk of a speciating change spreading through the population. If the mutant cannot breed, the genetic change it carries cannot spread. The only possible way speciation can occur under current evolutionary theory is through ignoring the source of the change being from individuals and implying that it is a very gradual set of changes happening not in actual organisms but only in populations. It is an absurd and unreasonable abstraction.

Even with all of the hemolytic factors involved in Rh differential pregnancies, there is no guarantee of death of the fetus or newborn thus the breeding is successful in these individuals. Were that not the case, we would not see such widespread variation in serology. There is no absolute need for medical intervention as the hemolytic issues vary widely from extreme(where miscarriage is the result) to so mild that there is no noticeable affect on the offspring.

The success of the mutation affecting RH factor demonstrates this, that mutational speciation does not 'fit' with evolutionary gradualism.

As I describe above, I honestly don't think this is the case. It's not as if Rh factors have created a speciation event.

This does not invalidate evolution. It just shows that the current accepted system is too simplistic and missing alternate mechanism/s (in my opinion). For example, one solution might be the simultaneous mutation of several compatible speciated individuals. Say from a mutation induced by a virus or targeted toxin ('gene shears' being one such actual laboratory example).

except that if you're talking about a speciation event, then the individuals would not be compatible.

If they carried the identical mutation, they would be bio-compatible with each other and could form a breeding colony. They would be a new species.

Is it impossible that identical mutation would arise in a number of individuals at the same time? No.

Could a mutagenic factor affect a number of individuals in exactly the same way? Yes.

Much of what we do when we manipulate genetics are natural processes but these natural processes are noticeably absent from evolutionary theory.

Which ones? just trying to make sure I'm following you clearly here and not make an assumption.

The horizontal transfer of genetic attributes from one species to another.

Monsanto did it to soy and are doing it to other crop species (RoundUp Ready crops). They found an organism living in a waste pipe leading out of their factory that produced the RoundUp (glyphosate) herbicide. It was successful as an organism in that environment because it had resistance to glyphosate.

They identified the resistance gene, extracted and concentrated it and then inserted it into firstly soy, and then other crop plants.

Every process they used to do this, occurs in nature. Humans have been doing the genetics engineering thing for such a short time compared to nature.

We have simple reasonable and demonstrable examples of how genetic change may occur that are just not considered in evolutionary theory!

And they would be?

Horizontal genetic transfer.

So, we must conclude, it is incomplete.

I don't know any Anthropologists or Evolutionary Biologists who would realistically disagree with that statement. One must keep in mind though that what is discussed is typically what is known for certain currently, things that can be demonstrated to be true. If there is more out there and the data supports it, current views on evolution will change just like it was contentious 20 years ago to say that Humans bred fertile offspring with Neandertal and it is currently an accepted fact.

(Gets off soapbox. Please excuse my rant but it was slightly on topic).

Rant away! An exchange of ideas is never a negative thing if either side is willing to learn something from it.

Apologies for the delay in my response. The the 'real world" intervened.

Here's something to think about, to get the gist of where I am coming from:

We all carry quantities of what is called "junk DNA", that is, gene sequences that do not seem to serve a function (that we know of).

The usual explanation of how they got into our genome is that they were transcripted in from RNA fragments, presumably carried into the cell by viruses.

So we end up with non-functional viral DNA, in our genome. That IS horizontal genetic transfer.

Perhaps, unbeknown to us, some of the viral DNA was actually functional and is part of what we assume to be human?

Where does modern evolutionary theory accommodate such horizontal genetic transfer?

Is horizontal genetic transfer any less likely than random mutation?

Now, if you accept that horizontal genetic transfer can, and does happen, then think about this hypothetical scenario:

An aquatic worm without eyes is living in an environment where there is another species, lets say an amphibian, that has eyes and has adapted them somewhat over time. Neither predates the other and they both have different food sources so they cohabit without any particular enmity.

Now the species with the eyes is affected by a virus which causes its death. The virus, due to its random genetic inefficiency when replicated ends up more than its own active RNA code, it carries a little bit more code stripped from the host organism at the time of cell rupture (i.e: the length of the RNA strand that will be carried by the virus is poorly defined).

It just so happens that the virus specifically binds its RNA into the segment of genome that is adjacent to the genes required for eyes (Perhaps there is some sort of preference for where the virus inserts itself into the hosts DNA).

So the Virus now carries the code for eyes.

Lets say it infects our blind species but is less successful in killing the organism (perhaps the success of the virus is moderated by the fact that this new host does not have the optimal gene sequence insertion point?). So now, when the virus infects the worm, it binds in its RNA which includes the code for eyes.

Subsequent generations of our once blind worm have eyes. Not partial and faulty but fully adapted and selected for. And it happened almost overnight.

This type of abrupt (saltational) change is actually observed and is the very reason that Punctuated Equilibrium is called upon as an explanation (but perhaps it is also not the only possible answer, as my little scenario may suggest).

When this is considered along with epigenetics (which makes Lamarckian ideas look less like idiocy), it is plain that evolutionary theory alone is inadequate, antiquated and incomplete.

a reply to: peter vlar

a reply to: chr0naut

So you need a Virus to cause the mutation ?

originally posted by: Temudjin
a reply to: peter vlar

a reply to: chr0naut

So you need a Virus to cause the mutation ?

Not necessarily.

A chemical toxin, ionizing radiation, heat shock or an electrical charge could cause a weakening of the transcription phase of DNA replication causing not just a simple mutation, but the binding in of alien (to the host) DNA fragments that have somehow penetrated the cell wall.

In the lab, we penetrate the cell wall with a pipette and introduce concentrated numbers of the specific genes we wish to add, then we usually use an electrical charge to cause the uptake of the new sequence.

The lab process usually adds a promoter region and a terminator region (like digital start and stop codes in computer communications) and a selectable marker/s to the sequence to be added to ease the genes insertion into the living genome. These are helpers in the transcription process but are not absolutely mandatory. They are added to the desired gene prior to injecting it into the host cell.

Viruses are simply convenient as they do a lot of the hard (genetic) work of transcripting into the live genome.

originally posted by: chr0naut
I am at a loss, as I cannot provide any examples of speciation that did not happen due to to the inability to breed. What evidence would there be for that? Perhaps you could provide some actually observed evidence of speciation occurring despite the speciated oganisms inability to breed, which would negate what I proposed?

And thats precisely my point. If its a single individual, its not an occurence of speciation. Speciation is measured across populations, it simply doesnt occur on an i dividual level in the way you describe. If a mutation makes it so thst someone can not mate with people directly descended from their forebearers they arent a new species as their genes will not be passed on.

Speciation can (and does) happen in a single step - a single mutation. There are many fetal immune related diseases that attest this (most survivable if the immune response of mother and child are suppressed).

Personally, I think you're being way too conservative with how you use speciation. No matter how you look at it, it is still a measure of population wide genetics. I'm an ardent supporter of Gould and Punctuated Equilibrium which was still fairly well frowned upon in the 90's when I was in school and which I took a lot of flack over. But speciation still does not occur on an individual level.

It is nonsense double-think to talk of a speciating change spreading through the population. If the mutant cannot breed, the genetic change it carries cannot spread. The only possible way speciation can occur under current evolutionary theory is through ignoring the source of the change being from individuals and implying that it is a very gradual set of changes happening not in actual organisms but only in populations. It is an absurd and unreasonable abstraction.

Not nonsense or double talk at all, as I mention above, its not a new species if it cant spread its genes. Youre speaking of spreading genetic change while insisting a speciation event occurs on an individual level despite the mutated individual in your exemplar being incapable of producing offspring. I see what youre getting at eith the i ability to produce offspring meaning its a new species but youre being far too oedantic in your interpretation of a speciatiin event. Speciation is defined in changes in populations though, not individuals(i know Im besting a dead horse at this point) but soeciatiin is in fact defined as I describe it. It is drfined specifically as the formatiin of new species as a resukt of geographic, physiological, anatomical or behavioral factors that prevent previously intervreeding populations from breeding with each other. One random individual with mutations that make them incapable of breeding does not a species make. If thst were the case, all infertile men and women would be classified in a seperate taxonomy.

As I describe above, I honestly don't think this is the case. It's not as if Rh factors have created a speciation event.

Then I simply misunderstood what you were grtting at there. My apologies.

If they carried the identical mutation, they would be bio-compatible with each other and could form a breeding colony. They would be a new species.

Is it impossible that identical mutation would arise in a number of individuals at the same time? No.

Could a mutagenic factor affect a number of individuals in exactly the same way? Yes.

And what examples can we cite to support this? In regards to evolution, i wont ever say anything is impossible. I will however demand evidence to support a hypothesis that is contrary to what is known currently. It would be bad science to simply accept it at face value. Its not anything personal against you, i swear!

The horizontal transfer of genetic attributes from one species to another.

Monsanto did it to soy and are doing it to other crop species (RoundUp Ready crops). They found an organism living in a waste pipe leading out of their factory that produced the RoundUp (glyphosate) herbicide. It was successful as an organism in that environment because it had resistance to glyphosate.

They identified the resistance gene, extracted and concentrated it and then inserted it into firstly soy, and then other crop plants.

Every process they used to do this, occurs in nature. Humans have been doing the genetics engineering thing for such a short time compared to nature.

There are certainly similies in nature but you cant honestly compare laboratory genomics to natural processes thst arent on purpose.

Horizontal genetic transfer.

But there isnt a question about the affects of horizontsl or lateral gene transfer in evolutionary theory. Im not sure where you get thst impression. Its well understood in single celled organisms to be the primary mover of genetics. Just because its not the defacto hypothesis for mukticellular, i.e. Animals in this instance, doesnt mean its not understood to occur. Im just not terribly comvinced of its i fluende on humans. There was a rather prominent study done not long ago thst represented the completelness of the study a bit errantly. Just my opinion but tge science does support it. The study had very incomplete representstion of the HAS1,HAS2, and HAS3 genes specifically yet puts it out as if these genes are fully represented in the tree for example. I would go into a little more detsil but Ive got a 7 year ild demanding some time rt now but I will be back to address your further comments.

Apologies for the delay in my response. The the 'real world" intervened.

No appologies necessary. Life always gets in the way when hou least expect it.