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in case it isn't obvious i'll begin by stating that i'm a layman, trying to understand something about this subject from reading books. the books i've looked at so far give murky and confusing accounts of meiosis (example: a schaum's outline refers to chromosomes that are "identical, but not the same"), and they always seem to duck the questions i most want answered. what i'm reaching for right now is a coherent, schematic understanding of meiosis. i'm aware that the real world is messier than that, but there clearly is a simple schema that accounts for the most typical cases of meiosis in an approximative fashion. in particular, there must be some way of deriving the approximate correctness of mendelian independent assortment of alleles from the molecular process of recombination.

here's what i think i can make out so far: if two chromosomes x1...xn and y1...yn get paired together then some number of interstices (spaces between successive loci) get picked and each chromosome gets broken at each interstice. after crossover each of the two resulting chromosomes have x-segments alternating with y-segments. for example if only one interstice is picked, and it's between the k-th and (k+1)-th loci, then the chromosomes that are there after crossover are x[1]...x[k] y[k+1]...y[n] and y[1]...y[k] x[k+1]...x[n]. it also seems clear that all interstices are equally likely to get picked. have i got at least this much right? and if so, how many interstices get picked?

also, if anyone knows a book that might suit my needs i would obviously be glad to hear about it. thanks if you can help

peace stm

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  • $\begingroup$ Homologous recombination does not occur randomly at every locus and thus independent assortment really only holds for genes that are far apart or on different chromosomes. $\endgroup$ – canadianer Aug 25 '14 at 6:49
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Parts of your general idea are correct, others need some refinement. To skip ahead to the conclusion: I'm going to recommend that you read up about linkage disequilibrium. Everything else is background information that will hopefully help you understand why linkage disequilibrium is what I think you're looking for.

Background: Meiosis Basics

Firstly, in the bare principle, meiosis is quite simple. Let's consider meiosis in a human cell, i.e. the division of a primary spermatocyte (the only other example is division of primary oocytes). That's this one we're talking about: http://en.wikipedia.org/wiki/File:Figure_28_01_04.jpg In simple terms, the ready-to-develop primary spermatocyte contains 46 chromosomes, two (2n) each of chromosomes 1-22, an X and a Y chromosome. Two chromosomes of the same type (e.g. "chromosome 4") are called homologues. Homologues contain different versions (= alleles) of the same genes. During Meiosis I, homologues align in pairs, recombine, and then separate into two new cells (which are now 1n). The following Meiosis II is basically a mitosis, meaning that the two (identical apart from previous recombinations) chromatids of the chromosomes are separated and packaged into separate cells.

Recombination and Interstices

During the alignment of homologues in Meiosis I, the attraction between the two chromosomes depends on their homology - i.e. similarities in DNA sequences that end up being close to each other in this setting. This attraction is on the molecular level, so the tightly-condensed neighbouring DNA double-helices actually physically stick to each other because the polarities/charges across relatively large stretches of the molecules complement each other. I don't think how this exactly works is well understood yet, but what is clear is that homologues attract each other at this point because they contain mostly the same DNA sequence, apart from small differences (which make the different alleles).

How exactly recombination occurs at this point isn't entirely clear either on the molecular level (http://en.wikipedia.org/wiki/Homologous_recombination#In_eukaryotes). Just to get an idea of how it could work: while the two chromosomes are aligned, it's not difficult for them to actually tangle up and break, leaving the repair machinery with the potential to fuse the wrong chromosome ends together. The breaking and exchange might also be a programmed process with dedicated cell machinery (quite probably so I think personally).

In any case, not all locations are equally likely to recombine. It depends on levels of homology (i.e. "stickiness") between individual stretches of DNA and other unknown factors. Just in the same way, the number of break points in each chromosome isn't pre-determined.

Mendelian Inheritance

First of all, the concept of loci is arbitrary and has no molecular basis. A locus is simply "a place on a chromosome" and could refer to an individual base(-pair) or a whole stretch of DNA. The concept is however useful when talking about inheritance, as it illustrates the principle of linkage, or rather linkage disequlibrium.

As far as I am aware, it comes from a time before we began thinking in chromosomes. One could study whether there was linkage between two traits (or more generally loci), i.e. a higher-than-random chance to inherit the two together. We now know that linkage simply means that the two loci are on the same chromosome (for example, chromosome 6). Thus, if no linkage exists, the chance to inherit both loci together is no larger than expected by random Mendelian inheritance (which makes sense as there is no molecular mechanism that makes offspring e.g. more likely than 50/50 to inherit chromosome 6 and 19 together from the same parent). If linkage exists , the loci are on the same chromosome, and any case where the two are not inherited together must be caused by recombination.

The idea of linkage disequlibrium is that loci that are close to each other on a chromosome are more likely to remain together (and be inherited together) than far-apart loci. This is obviously due to the increased chance of a recombination event occurring between them with increased distance. This actually seems to be what you are looking for as a pointer for where to go next, so I recommend using your preferred internet search engine to learn more about that :)

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some number of interstices (spaces between successive loci) get picked and each chromosome gets broken at each interstice.

That number is usually around 1. It's not common to have a lot more than that per chromosome.

It also seems clear that all interstices are equally likely to get picked.

No, there certainly are "hot spots" that are more likely to be cross-over junctions than other sequences.

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