VerticalHairFactor wrote:Dragi forumaši, naletio sam na sljedeće:
...
Dakle, genetika obara teoriju evolucije.
1) Nemoguce je da mutacijom nastane novi gen. Najprostija bakterija ima 500 covjek preko 22.000
2) Nemoguce je zamjeniti genetski materijal mutacijama u tolikoj mjeri da se sa jednocelijskog nezavisnog sistema predje na visecelijski zavisni organizam.
3) Nemoguce je ispuniti prvi i drugi uslov i jos da se to dogodi dvaput istovremeno kako bismo imali muzjaka i zenku.
Može li se neko "očitovati" o gore spomenutom, u smislu da mi da odgovor, ukoliko postoji, na navedene tvrdnje o "genetika vs evolucija".
Druze, moram priznati da si me iznenadio, a pomalo i razocarao, priznat cu, iz razloga jer mislim da si kud i kamo sposobniji pronaci relevantnu informaciju ticanu za problematiku koju navodis u svom pitanju. Al' hajde, neise, sto bi rekli. Podjoh kvotati tvoj posti da bih ti ukazao na pogresne premise vezane za specijaciju generalno i evoluciju iz jednocelijskog u visecelijski organizam konkretno, kao i to da novi geni unutar genoma ne nastaju mutacijama, sto ces i sam vidjeti u par citata ispod, ali, posto nisam bas s vremenom, odlucih ti postaviti par clanaka ljudi iz struke koji bi ti trebali ponuditi dgovore na tvoja pitanja:
(Posljednji clanak u nizu se konkretno bavi tvojim pitanjem dok su ostali, dosta strucniji radovi, kontekstualno druge prirode ali se primarno temelje upravo na toj
genetskoj duplikaciji koja je u genetici zapravo jedan od primarnih mehanizama uz rekombinaciju i mutacije, a koja je odgovorna upravo za ono sto te zanima.)
Gene. 1999 Sep 30;238(1):103-14.
Genome evolution and the evolution of exon-shuffling--a review.
Patthy L.
Institute of Enzymology, Biological Research Center, Hungarian Academy of Sciences, Budapest.
[email protected]
Recent studies on the genomes of protists, plants, fungi and animals confirm that the increase in genome size and gene number in different eukaryotic lineages is paralleled by a general decrease in genome compactness and an increase in the number and size of introns.(...)
http://www.ncbi.nlm.nih.gov/pubmed/10570989
(ako ne mozes pronaci cijeli clanak javi)
Genome increase as a clock for the origin and evolution of life
Alexei A Sharov
(...)Although the global increase of genome sizes from bacteria to mammals is a well-known fact, no attempt has been made to model this process. The total genome size appeared highly variable among organisms with the same level of morphological complexity, a phenomenon known as a C-value paradox. These variations in genome size are caused mostly by gene duplication, polyploidy, and accumulation/deletion of intergenic DNA. Thus, genome size was mostly studied as an indicator of insertion-deletion frequencies in different species rather than a measure of complexity.
Biological complexity was recently defined by Adami et al. as a size of functional and non-redundant genome. This measure does not depend on duplications, insertions, or deletions of non-functional or redundant sequences, and therefore it is more stable in evolution than the total genome size. The dynamics of genome increase in evolution can be modelled on the basis of known mechanisms which appear to act as positive feedbacks. First, the theory of a hypercycle considers a genome as a community of mutually beneficial (i.e., cross-catalytic) self-replicating elements. For example, a gene that improves proof-reading increases the replication accuracy of all other genes. These benefits are applied not just to existing genes but also to genes that may appear in the future. Thus, already existing genes can help new genes to become established, and as a result, bigger genomes will grow faster than small ones. Second, new genes usually originate via duplication and recombination of already existing genes in the genome. Thus, larger genomes provide more diverse initial material for the emergence of new genes. Third, large genomes support more diverse metabolic networks and morphological elements (at various scales from cell components to tissues and organs) than small genomes, which in turn may provide new functional niches for novel genes. These three mechanisms of positive feedback may be sufficient to cause an exponential growth in the size of functional non-redundant genome.(...)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1526419/
Riedl’s Theory
Riedl’s (1977) theory for the evolution of “genome systemization” is the main earlier example of a constructional selection theory for the genotype-phenotype map. He considers the situation where functional interactions arise in the organism that require the coordinated change of several phenotypic characters in order to produce adaptive variants.
When this would require simultaneous mutations at several genes, he argues that the evolution of a new gene that produces the needed coordinated variability — a “superimposed genetic unit”—is a far more likely possibility. Thus Riedl is proposing that the genotype-phenotype map can evolve in directions that facilitate adaptation through selective genome growth.
http://citeseerx.ist.psu.edu/viewdoc/do ... 1&type=pdf
Where do new genes come from? Although there is a certain amount of de novo synthesis of DNA in the genome, most genes originate from template based duplication of existing sequences. And while the vast majority of gene duplications may go to extinction, the genes currently functioning in an organism will possess an unbroken backward genealogy to earlier, ancestral genes (complicated perhaps by the occasional reactivation or insertion of pseudogene sequences). So there exists an “intra-genomic phylogeny”, which is actually beginning to be taken as an object of study as the accumulation of DNA sequences allows the construction of “gene-trees” (Dorit and Gilbert 1990, Dorit et al. 1991, Strong and Gutman 1992, Burt and Paton 1992, Klenova, et al. 1992, Streydio et al. 1992, Haefliger et al. 1989).
http://citeseerx.ist.psu.edu/viewdoc/do ... 1&type=pdf
Gene duplication
Evidently the total information capacity of genomes is very variable across the living kingdoms, and it must have changed greatly in evolution, presumably in both directions. Losses of genetic material are called deletions. New genes arise through various kinds of duplication. This is well illustrated by haemoglobin, the complex protein molecule that transports oxygen in the blood.
Human adult haemoglobin is actually a composite of four protein chains called globins, knotted around each other. Their detailed sequences show that the four globin chains are closely related to each other, but they are not identical. Two of them are called alpha globins (each a chain of 141 amino acids), and two are beta globins (each a chain of 146 amino acids). The genes coding for the alpha globins are on chromosome 11; those coding for the beta globins are on chromosome 16. On each of these chromosomes, there is a cluster of globin genes in a row, interspersed with some junk DNA. The alpha cluster, on Chromosome 11, contains seven globin genes. Four of these are pseudogenes, versions of alpha disabled by faults in their sequence and not translated into proteins. Two are true alpha globins, used in the adult. The final one is called zeta and is used only in embryos. Similarly the beta cluster, on chromosome 16, has six genes, some of which are disabled, and one of which is used only in the embryo. Adult haemoglobin, as we’ve seen contains two alpha and two beta chains.
Never mind all this complexity. Here’s the fascinating point. Careful letter-by-letter analysis shows that these different kinds of globin genes are literally cousins of each other, literally members of a family. But these distant cousins still coexist inside our own genome, and that of all vertebrates. On a the scale of whole organism, the vertebrates are our cousins too. The tree of vertebrate evolution is the family tree we are all familiar with, its branch-points representing speciation events — the splitting of species into pairs of daughter species. But there is another family tree occupying the same timescale, whose branches represent not speciation events but gene duplication events within genomes.
The dozen or so different globins inside you are descended from an ancient globin gene which, in a remote ancestor who lived about half a billion years ago, duplicated, after which both copies stayed in the genome. There were then two copies of it, in different parts of the genome of all descendant animals. One copy was destined to give rise to the alpha cluster (on what would eventually become Chromosome 11 in our genome), the other to the beta cluster (on Chromosome 16). As the aeons passed, there were further duplications (and doubtless some deletions as well). Around 400 million years ago the ancestral alpha gene duplicated again, but this time the two copies remained near neighbours of each other, in a cluster on the same chromosome. One of them was destined to become the zeta of our embryos, the other became the alpha globin genes of adult humans (other branches gave rise to the nonfunctional pseudogenes I mentioned). It was a similar story along the beta branch of the family, but with duplications at other moments in geological history.
Now here’s an equally fascinating point. Given that the split between the alpha cluster and the beta cluster took place 500 million years ago, it will of course not be just our human genomes that show the split — possess alpha genes in a different part of the genome from beta genes. We should see the same within-genome split if we look at any other mammals, at birds, reptiles, amphibians and bony fish, for our common ancestor with all of them lived less than 500 million years ago. Wherever it has been investigated, this expectation has proved correct. Our greatest hope of finding a vertebrate that does not share with us the ancient alpha/beta split would be a jawless fish like a lamprey, for they are our most remote cousins among surviving vertebrates; they are the only surviving vertebrates whose common ancestor with the rest of the vertebrates is sufficiently ancient that it could have predated the alpha/beta split. Sure enough, these jawless fishes are the only known vertebrates that lack the alpha/beta divide.
Gene duplication, within the genome, has a similar historic impact to species duplication (“speciation”) in phylogeny. It is responsible for gene diversity, in the same way as speciation is responsible for phyletic diversity. Beginning with a single universal ancestor, the magnificent diversity of life has come about through a series of branchings of new species, which eventually gave rise to the major branches of the living kingdoms and the hundreds of millions of separate species that have graced the earth. A similar series of branchings, but this time within genomes — gene duplications — has spawned the large and diverse population of clusters of genes that constitutes the modern genome.
The story of the globins is just one among many. Gene duplications and deletions have occurred from time to time throughout genomes. It is by these, and similar means, that genome sizes can increase in evolution. But remember the distinction between the total capacity of the whole genome, and the capacity of the portion that is actually used. Recall that not all the globin genes are actually used. Some of them, like theta in the alpha cluster of globin genes, are pseudogenes, recognizably kin to functional genes in the same genomes, but never actually translated into the action language of protein. What is true of globins is true of most other genes. Genomes are littered with nonfunctional pseudogenes, faulty duplicates of functional genes that do nothing, while their functional cousins (the word doesn’t even need scare quotes) get on with their business in a different part of the same genome. And there’s lots more DNA that doesn’t even deserve the name pseudogene. It, too, is derived by duplication, but not duplication of functional genes. It consists of multiple copies of junk, “tandem repeats”, and other nonsense which may be useful for forensic detectives but which doesn’t seem to be used in the body itself.(...)
By Richard Dawkins
http://www.skeptics.com.au/publications ... challenge/
Takodjer, potrazi knjigu
Evolution by gene duplication, Susumu Ohno (1970) i proguglaj
Gene duplication.
Dakle, geneza novog gena unutar genoma je prilicno jasan i vec duze vremena obimno istrazen fenomen.
