UPDATE: The authors of this paper were rather upset by my initial description of it, so I will just say that I found it very confusing and leave it at that. See the abstract below and check out the paper if you are interested.
Freeling, M.W., Xu, J., Woodhouse, M., and Lisch, D.R. (2015). A solution to the C-value paradox and the function of junk DNA: the Genome Balance Hypothesis. Molecular Plant, in press.
The Genome Balance Hypothesis originated from a recent study that provided a mechanism for the phenomenon of genome dominance in ancient polyploids: unique 24nt RNA coverage near genes is greater in genes on the recessive subgenome irrespective of differences in gene expression. 24nt RNAs target transposons. Transposon position effects are now hypothesized to balance the expression of networked genes and provide spring-like tension between pericentromeric heterochromatin and microtubules. The balance (coordination) of gene expression and centromere movement are under selection. Our hypothesis states that this balance can be maintained by many or few transposons about equally well. We explain known, balanced distributions of junk DNA within genomes, and between subgenomes in allopolyploids (and our hypothesis passes “the onion test” for any so-called solution to the C-value paradox). Importantly, when the allotetraploid maize chromosomes delete redundant genes, their nearby transposons are also lost; this result is explained if transposons near genes function. The Genome Balance Hypothesis is hypothetical because the position effect mechanisms implicated are not proved to apply to all junk DNA, and the continuous nature of the centromeric and gene position effects have not yet been studied as a single phenomenon.
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