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Fig. 2. Schematic representation of MSCI. (A) During leptotene,
widespread ATM-dependent H2AX phosphorylation occurs in response to
meiotic-DNA DSB formation. BRCA1 and ATR form foci on newly forming axial
element (AEs). (B) During zygotene, synapsis coincides with the loss of
BRCA1, ATR and 
H2AX from autosomal AEs. BRCA1, ATR and H2AX
remain as foci on the AEs of autosomes that have not yet synapsed and on the
AE of the X chromosome. (C) Zygotene-pachytene transition. Autosomal
synapsis is complete and recombination-related H2AX disappears. BRCA1-
and ATR-staining becomes linear on the X and Y AEs. Meiotic DNA is arranged in
loops attached at their bases to the AEs. (D) Early pachytene. ATR
translocates along DNA loops, where it phosphorylates H2AX, resulting in MSCI
and in the formation of the sex body. (E) Mid-to-late pachytene. Other
histone modifications [e.g. the production of H3K9me2, uH2A and histone
variants (e.g. H2AFY)] ensure the maintenance of MSCI. (F)
Diplotene-to-diakinesis. The X and Y chromosomes migrate to the centre of the
nucleus. BRCA1, ATR and H2AX are lost from the X and Y chromosomes, but
the other modifications remain. These modifications ensure the maintenance of
MSCI throughout the meiotic divisions (G) and into spermatids
(H), and is termed post-meiotic sex chromosome repression (PSCR).
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