dttom

Should we equating 'using tools' in human and that in chimps? If they are equal, then yes, by parsimony it is plausible to deduce the LCA also did the same. But I suspect they are not equal, and largely invented (evolved) independently. If two are not equal, parsimony no longer support the argument.

It should be: 1) Eubacteria 2) Arhaea 3) Eukaryotes Protists disperse into eukaryotes.

Blood for them is just a sort of nutrient source, comparable to human drinking nutritious drinks, and insect blood and the host blood they feed on are not mixed, host's blood gets straight to their digestive system, useful nutrients absorbed, wastes remained. Krebs' cycle is character rooted deep into evolutionary history of life, insects have the same Kreb' cycle mechanism as we have. And for the iron metabolism of course they should be different, but seems to be unrelated to hematophagy, the hemolymph or insect blood does not contain hemoglobin yet with ions.

Both iron compounds in oxidation state of +2 or +3 are stable. Depending on its chemcial and physical environment they would interchange in some cases. Like a iron (II) compound like FeSO4 if left in air it would be converted to iron (III). If you want to know if an equation you have written is feasible in energetical terms, just check up the reduction potential table. If you want to make iron from its +3 state back to +2 state it has to be the cathode and undergoes reduction. But probably this question should not belong to 'organic chemistry' session...

Tissues are regarded as 'non-self' if it is present by nonself MHC. Class I MHC activates Tc lineage and class II MHC activates Th lineage, the former requires support from the latter. When class I MHC is recognised by a Tc cell and it differientiates to CTL with the help from Th cell after recognising foreign class II MHC. CTL attacks and rejects the transplant. The process is also accompanied by B cell lineage attack involving Ig as well as complement system.

1) Yes, for class II MHC; and yes for class I MHC too if 'beta chain' means beta-microglobulin. 2) Yes. 3) Yes.

Even if B cells contain CD45R and CD45R is found to have interaction with CD22 does not imply B cells would interact with all cells expressing surface CD22. Interaction might requires other intermolecular adhesion. And CD22 is present in B cells, so it actually suggests the APC role of B lineage.

I'm afraid I should say sperm could hardly tell how to form the embry, nor is it sharing 50% of the work. Spermatozoan, definitely a cell, but its size is too small to have significant cytoplasm, this is of evolution reasons, involving intersexual competition which is not the focus. Though spermatozoan carries 50% of the constituting genome of the would-be embryo, it would be meaningless if there is no guide to illustrate how such half a genome is used. Little difference in genomes between species suggests primary sequencial genomic difference might not be the only rationale is constructing so different species, and it is. The paramount is how the cell, being totipotent, is guided to express the 'required' proteins in a 'proper' manner and sequence. Homeotic genes play an essential role, particularly famous, the Hox genes. That's why I said sperm does less than the egg which has a large cytoplasm to include differential chemical concentration gradient, switching Hox genes in 'proper' region and determine the anterior/posterior dimension the early embryo.

Widdekind was telling that haemoglobin in arthropods, when oxygenated, is in blue. And actually not only in arthropod, crustacean like lobster, various crabs appears to stain the ice below blue in wet market. If it is using copper in the haemoglobin it should be blue in oxygenated form, blood in mammals appears red as iron instead is exploited. Back to the question, indeed I got a question, how could you relate blue blood and oxygen scattering short wavelenght light? For me I can't see the direction relationship, the facts you suggested are alright to me, but two should not be linked in this way.

Maybe there could be a gene laid silent during most of the lifetime but could be triggered to express, once expressed it poisons the spliceosome and render it non-functional. Approaches could be attempt like this. But I suspect the experimental organism would be badly affect after such an induced expression, spliceosome modifies hnRNA to give mRNA, by cutting out introns guided by sequence signal before and after intron region, potentially many stop codons or start signals could be included, without cutting out the intron the RNA could even not be exported out of nucleus as it lacks certain signalling molecule attached (EJC if I remember it rightly). Even it makes it way to the cytoplasm, I bet it couldn't be translated into functional protein as usual, hindered by the stop codon and start signal in the introns, matter is further complicated by potential regulatory sequence in intron region, where molecule could bind and affect translation.

A protein contains a series of peptide bonds which are alpha peptide bonds, as their linkage are made between alpha nitrogen and carbon 1. Lysine contains a side group with an amine functional group, which could form another type of peptide bond, such is not an alpha peptide bond as it is not adjacent to carbon one, it should be an epsilon peptide bond.

It should be alright for the somatic ones, and telomerase works on germ line and special lineages (those rapidly divide) to replenish the telomere.

The carbon adjacent to the carbon 1 is the alpha carbon.

You are right in memetic terms. I don't deny there are, and should be, some cross-relationship between this kind of evolution, or rather cultural evolution and the genetic evolution, but if it is to say memetic is taking more importance and showing a trend in replacement I'm afraid it would never be the case as long as an organism relys on genetics for existence.

May I ask why you want to insert it into lettuce? If you think this could insert the insulin gene into a patient that would probably not work as the insulin gene should be digested before absorption, even it is injected directly into blood I just can't see how it would incorporate itself into cells' genomes, and probably into certain cells' genomes.

The gene should never adapt in a single individual on environment stimuli or epigenetic changes. Yet it is because the expression patterns or modes are different so as to bring about an epigenetic change. This would depends on the interpretation of 'Stress'. If it is interpreted as any environmental stimulus which on average causes a particular set of symptoms, it surely should not conscious. But if it is known as any environmental stimulus which causes a particular set of symptoms on an individual, it would largely depend on how that one perceive the same stimuli, then it could be conscious, though with objective factors. Back to the issue, for me I would believe it as possible. But if one would like to dissect why it is the case on molecular level or by any scientific analysis, the logic breaks down. If the question is how one's body is, it could further be asked that who is perceiving the body. If the perceiver think, believe, no matter which word with the same meaning, the mode of the body, the body would just be that. Probably this answer is confusing to many, so let's go back to more understandable scientific thinking. I suspect, one could change the body state to a point, but not all; the mindset or conscious mind is controlled by the central nervous system, and there should be a point limit, like it is limited by the hardwiring of the nerves, to where the CNS could control obeying the physiochemical principles.

You remind me that there is a circumstance that the food source which the usual individuals choose is completely alternative, that choice on other food source would not result in lowering in fitness, except, if it is a social species the alternative food source would, if any, posed some social barrier which lowers its competivity. And the inbreeding issue, I think there should be, and to a certain degree is a must accompanying to any speciation event. The founder effect based on geographic isolation would still meet the same problem. But of course, any speciation is the result of the sucessful passing through of such a bottleneck. Going through such an event relatively short ago is also why the human genome diversity is limited compared with other species.

Early in the human history, when the individual could hardly be rendered as human by modern standard, wars or conflicts between tribes were usual. The idea that a member should contribute the tribe but not the rivaling tribe was necessary for sustaining the glory of a tribe. This resulted in the basis for the religion that a member should have as little relationship with a member from other opposing tribes. Punishment was expected for those who betrayed this meme. Under such a condition, a member who remained ‘loyal’ to his tribe would be credited and the opposite would be disregarded, and this would easily favor the emergence of gene, if any, which distinguished between members of his own tribe and those of the opposite, as one could be innocently punished by accidentally recognizing ‘foreign’ as ‘self’. With the emergence of such a gene, or genes, the accident rate and innocence were expected to decrease, though such genes could confer virtually no benefit for those who were loyal, yet they could still spread through genetic drift. Coupled with civilization, such a meme declined, yet the ‘loyal’ genes persisted. This could be one of the results of the differential emergence rates between memes and genes, both being an element in respective evolution. Such a ‘loyal’ gene would instinctively suggest a person to favor ‘self’, or of his own kind, which simultaneously and relatively suggest disfavoring ‘non-self’ or other kinds. The word ‘self’ in ancient time was defined as members in a tribe which the individual belonged to, and this gene worked by allowing an individual to recognize characteristics shared amongst members within the same tribe yet not possessed by those outsiders; inferring its meaning it could easily mean the individuals sharing the same recent ancestry with the possessing individual. Such an ancestry would surely be very recent. Yet would this form the basis for the especially irritating race issue is an open topic for discussion, though until today there has not been a gene identified for ‘discriminatory’. Another separate example in this issue is related to insects. In some species of insect imprinting plays a determining role in the food source which the larvae and the grown-up adult would eat by selecting the location where to lay the eggs. For an individual accidentally laying eggs in a ‘wrong’ location could drive an offspring lineage to a different food source. Because of difference distribution of food, this accident could become a sympatric barrier and drive the subsequent genetic evolution. The process of imprinting is definitely not a genetic one, the action would not change even a tiny bit in germ-line genome; if considering it as epigenetic would also be sensible as the process should at least involve some changes in cell connection, signaling or synthesis in chemicals in vivo; yet it would also make sense if treating it as a kind of vertical meme base on the same logic, meme propagation should provoke some in vivo change for it to function, as no signal could transmit without contact.

The sequence is not necessary to be mRNA first then miRNA and RISC formation, it could be reversed so the activity of the later transcribed mRNA is controlled, says if the RISC recognises that mRNA and binds to and degrades it, but there is still a portion of which has yet been degraded, in addition to transcription of mRNA. So activity of mRNA is regulated. A copy of miRNA could bind not only to one species of mRNA so there is a potential of a diversity in cross-regulation. To your thought that scientists before 90s have not thought about a regulatory mechanism for mRNA functioning, I'm not sure, but it should be more plausible if you considered they have not found such a mechanism.

True that it's hygroscopic; but it should also be dehydrating to draw water out from carbohydrates.

If it is 'memeone', then I suspect the case would be a bit different. In traditional gene selection, natural selection force acts on individual by 'death or live', hence for each turn of selection the unit would be genomic. But in the case of meme, each turn of selection should actually be within single society before two societies could be selected against. If a society containing a set of meme that is inferior to another set of meme within another society, assuming there is no meme flow, there should come first meme selection then memeone selection (society selection), in other words, the vanish of one society should follow a series of meme selections. So in this case I believe memeonic selection is a result of long-term meme selection provided with long enough period of time for serial meme selections to effect in a system with certain degree of meme isolation. However, the case becomes very different if taking meme flow into consideration. As each turn of selection acts on meme scale, one can use a model that favorable meme would have higher propagation rate, as this meme propagation could flow freely between societies, or meme pools. Here provides no chance for memeonic selection, just as if there would not be speciation if no isolation force exists (speciation similar to divergence in meme pools, or societies). This model bases on totally free meme flow, which exists only theoretically, yet in reality the situation is coming closer and closer to this limit with the advance in information electronics (we are now using this forum to share ideas...).

I think the reason why evolutionary models could be derived on the gene level is basing on the assumption that there were enough time for genes to resolve so as to be considered as a single unit for selection (otherwise I think they would be selected in a unit of gene assembly). And not only the case of population study I think in all case the unit for each turn of selection should on the level of individual, or genome. Provided with long enough period of time, the phenotypic unit of selection will shift from genome to gene assembly, then to gene itself. Merged post follows: Consecutive posts merged Yes I think the idea described by Mr Skeptic is about meme. And I do think this has exerted a prominant effect on haminity and culture evolution.

Cancer is the malignant proliferation of cell, so if there are more information about which proteins are functioning in cell division and their expression pattern, probably you would have a glance at the potential cancer treatment.

So the no.320 nucleotide got a point mutation, if you do the calculation of 320/3 you get the remainder 2, it counts from 319 to 321 as one codon, so you need to check what the amino acid should be and what it has become now.

As CharonY has suggested, some of my points about the evolutionary selection unit in my previous thread titled 'About mutualism between human and E.coli' would be described here and for open discussion. The main idea is that I believe the selection unit is not fixed over the evolutionary time, instead, the level of this unit could change depending on circumstances. One of the important factor should be period of time available for resolution of a gene from its corresponding bundle (gene assembly). The statements about this point was quoted from my previous thread as below: "I should agree that for each time of selection (who dies, who lives), natural selection acts on individual level, so at genomic level; however, in long run, why shouldn't it act on genes' level, fostered by crossing over in meiosis? A complication arrives with speciation that, as genes in a genome are bundled together, if a gene could not be resolved (if a gene is resolved, it got the chances to be in different genomes (of course in different individuals) for natural selection) before microevolution occurs, probably the selection level could stay at a higher level than a gene. When talking about a gene could only exert its effect in a given genetic environment (together with other genes), as in the case of any individual, I have to admit that this is definitely the fact. But does this fact affect or change the consideration in selective level is another matter. For me this is a fact stating that a gene could have different effects in different combinations of genes (actually I would prefer, and better to, use the word gene assembly), but as long as a gene could be resolved, it got the chances to be in different genomes, and individual gene effect could be selected by natural selection. The result could be a gene might exert more advantageous effect when combining with a set of other genes (actually this is usually the case as a phenotype, no matter is the traditional definition of phenotype or the extended phenotype, is usually determined not by a single gene), in this case, such a gene assembly would be advantageous if they have a low COV relative to each other (harder to resolved from each other), ultimate result might be fusion to a single gene (please beware of the use of the word 'gene', not cistron, a 'gene' here could refer to a number of encoded polypeptides) which is selected later as single unit (this might be refered to by someone as an evidence to support the allegation of selection at a level higher than gene, so for me it is not a matter of concept but a matter of definition, view of phenomenon and explanation)."