Information Runs The Show — The Understatement of the Century!

PaV: If you are not familiar with those subjects, a good starting point would be to look in Wikipedia or a biology textbook for information on meiosis and homologous recombination. While those sources are not perfectly up-to-date, they will give you a good idea about the basis of those mechanisms. While I did study homologous recombination associated with DNA repair, I did not read many articles about the displacement of histones. What I can tell you though is that histones are not passively standing in the way during recombination: they actively participate during many steps. For instance, histone H2AX (which is involved in certain type of DNA repair) is important at least for the recruitment of specific proteins. The article “Genomic instability in mice lacking histone H2AX“ is a good example of the importance of this particular histone in DNA repair involving homologous recombination. While I do think I read that phosphorylation of H2AX was also associated with relaxation of the chromatin structure around sites of DNA damage, I don’t remember the title of the paper. Concerning the homologous recombination that happens during meiosis, I do remember some articles I read that you might find interesting: “PRDM9 Is a Major Determinant of Meiotic Recombination Hotspots in Humans and Mice” “Drive Against Hotspot Motifs in Primates Implicates the PRDM9 Gene in Meiotic Recombination” “Prdm9 controls activation of Mammalian recombination hotspots” Those 3 articles where published in Science in 2009. What they say is that the gene PRDM9 is associated with recombination hotspot (meaning that homologous recombination during meiosis is not entirely random). The gene could explain 18% of the variation in hotspot usage between individuals. The point that is very interesting is that the PRDM9 protein is involved in histone modifications which would also tend to support the idea that histones are directly involved in recombination (both during meiosis and during DNA repair) and not simply standing in the way. So the short answer would be: I don`t know for sure, but I do not think recombination have to occur between histones since they seem to be directly involved in recombination themselves. CharlesJ

Thanks Charles. I would suppose, since the chromosome is bound up around histones, that the natural linkage spots for recombination would occur somewhere in the region connecting one histone to another. Is that correct? Any good resources on all this? Any good reviews? PaV

PaV: Each allele is not on a single strand of DNA, it's on a double strand. We receive double stranded DNA from our mother and double stranded DNA from our father. Same thing with recombination: both strands are exchanged, so no problem of complementarity either. Aberrant pairing on complementary strands leads to a structure that is recognized by DNA repair mechanisms and is promptly removed. CharlesJ

Here's a link that gives a good overview of this article. I believe this is the "tip of the iceberg". I've often wondered how it is that DNA can combine strands which have different alleles. It would appear, on the surface, that the bonding would get all messed up unless the two strands, male and female, were exactly the same. DNA had to have a method to get around this mismatching. I suspect this Hoogsteen base-pairing might be intimately connected. As to neo-Darwinism, if it couldn't explain the functionality of Crick-Watson DNA, it hasn't a chance with this configuration, this "excited state". Another day, another bad day for Darwinism!!! PaV

Jonathan, you may find this interesting: Hoogsteen base pair Excerpt: History This term is named for Karst Hoogsteen, who, in 1963, first recognized the potential for these unusual pairings (quoted from Lehninger Principles of Biochemistry by David Nelson and Michael Cox, 4th edition, published in 2005 by Freeman). [edit] Chemical properties Hoogsteen pairs have quite different properties from Watson-Crick base pairs. The angle between the two glycosylic bonds (ca. 80° in the A• T pair) is larger and the C1?–C1? distance (ca. 860 pm or 8.6 Å) is smaller than in the regular geometry. In some cases, called reversed Hoogsteen base pairs, one base is rotated 180° with respect to the other. [edit] Triplex structures Base triads in a DNA triple helix structure This non-Watson-Crick base-pairing allows the third strands to wind around the duplexes, which are assembled in the Watson-Crick pattern, and form triple-stranded helices such as (poly(dA)•2poly(dT)) and (poly(rC)•2poly(rC)). It can be also seen in three-dimensional structures of transfer RNA. [edit] Quadruplex structures It also allows formation of secondary structures of single stranded DNA and RNA G-rich called G-quadruplexes (G4-DNA and G4-RNA) at least in vitro. It needs four triplets of G, separated by short spacers. This permits assembly of planar quartets which are composed of stacked associations of hoogsteen bonded guanines. [1] [edit] Triple helix base pairing Watson and Crick base pairs are indicated by a "•", "-", or a "." (example: A•T, or poly(rC)•2poly(rC)). Hoogsteen base pairs are indicated by a "*" or a ":" (example: C•G*G+, T•A*T, C•G*G, or T•A*A). http://en.wikipedia.org/wiki/Hoogsteen_base_pair bornagain77