In fruit flies, dosage compensation involves a 2-fold increase in expression of male X-chromosome genes (Prestel et al. 2010; Stenberg and Larsson 2011), supporting Ohno's hypothesis.
In fruit flies, dosage compensation relies on a male-specific molecular complex that binds to a short sequence of DNA found multiple times across the X chromosome (Conrad and Akhtar, 2011).
In flies, the dosage compensated X chromosome in males is characterized by increased acetylation of lysine 16 on histone 4 (H4K16ac), a hallmark of active chromatin (Turner et al. 1992).
Finally, removal of the MSL complex components does not result in halving of X chromosome gene expression relative to autosomes (Hamada et al. 2005; Deng and Meller 2006; Zhang et al. 2010), raising the possibility that other MSL-independent mechanisms may also contribute to dosage compensation in fly somatic cells.
If the mechanism underlying the male bias in fly and mouse is the same, it is unlikely, therefore, to directly involve dosage compensation.
Moreover, the recognition that distinct molecular mechanism underlay dosage compensation in flies, worms, and humans added further support to the universality of dosage compensation evolving concomitantly with differentiated sex chromosomes (Deng et al. 2011; Straub and Becker 2011).
The roX1 and roX2 (RNA on the X-1 and -2) are noncoding transcripts that play a central role in sex chromosome dosage compensation in flies.
Dosage compensation mechanisms in flies and mammals also utilize non-coding RNAs to nucleate the recruitment of chromatin modifiers that equalize the expression of X-linked genes (Wutz, 2011; Conrad et al, 2012).
Finally, percent Class F fly ash dosage can be expressed in Eq. (2) by taking natural logarithm in both sides of Eq. (1).
ASR-induced expansion of fly-ash containing mortar bars (Exp FA ) as related to control expansion (Exp CE ), immersion age (t) and Class F fly ash dosage (F) was evaluated, and the results were expressed in Eq. (1).
