Reciprocal constraints couple architectural protein abundance and pericentromeric satellite expansion.

In female mouse meiosis, HMGA2 abundance is linked to major satellite copy number, and reciprocal perturbations show each constrains the other in oocytes.

• Why it matters: Satellite arrays expand rapidly yet selective pressures limiting their growth are unclear; reciprocal constraints between satellite size and architectural protein levels could explain stability.
• What they did: Using the mouse major satellite, the study measured HMGA2 enrichment at major satellite and correlated HMGA2 expression with major satellite copy number in Mus musculus versus Mus spretus, then depleted or overexpressed HMGA2 in musculus/spretus hybrid oocytes.
• The result: HMGA2 depletion disrupted major satellite packaging in major satellite-rich musculus oocytes, while HMGA2 overexpression disrupted chromosome segregation in major satellite-poor spretus oocytes, supporting a co-evolution model of reciprocal constraint.

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