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Answer: In mammalian dosage compensation, particularly in female cells, one of the two X chromosomes is largely inactivated to balance the dosage of X-linked gene expression between males (XY) and females (XX). This process in female mammals is called X-chromosome inactivation (XCI) and involves the expression of a long non-coding RNA called Xist (X-inactive specific transcript). Xist RNA coats the X chromosome from which it is transcribed and initiates the formation of inactive heterochromatin.

The process goes as follows: 1. The Xist gene on the future inactive X chromosome (Xi) is upregulated. 2. Xist RNA spreads along the X chromosome in cis (meaning on the same chromosome from which it is transcribed). 3. The spreading of Xist RNA recruits various proteins and enzymatic complexes to the X chromosome. 4. These proteins include the Polycomb Repressive Complex 2 (PRC2), which adds the histone mark H3K27me3 (trimethylation of the lysine 27 on histone H3), signaling for chromatin to compact and become less accessible. 5. Additionally, hypoacetylation of histones (like reduced H4K16ac) happens on the inactive X chromosome, further promoting a condensed, inactive state. 6. These chromatin modifications lead to the formation of facultative heterochromatin, which results in the silencing of gene expression on the inactivated X chromosome.

The expressions "dosage compensation complex," "roX," and "H4K16ac" refer to components related to dosage compensation in Drosophila (fruit flies), not in mammals. In Drosophila, dosage compensation is achieved by upregulating the single male X chromosome to equal the expression of two X chromosomes in females, involving different mechanisms such as the male-specific lethal (MSL) complex that binds to the male X chromosome and increases transcription, partly by adding the acetylation mark H4K16ac.