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ATR is a multifunctional regulator of male mouse meiosis

Alexander Widger1, Shantha K Mahadevaiah1, Julian Lange2

  • 1Sex Chromosome Biology Lab, The Francis Crick Institute, 1 Midland Road, London, NW1 1AT, UK.

Nature Communications
|July 7, 2018
PubMed

Insights

The DNA damage kinase ATR is crucial for male mouse meiosis, regulating chromosome structure and germ cell survival during prophase I. Its absence leads to fragmentation and cell elimination, independent of ATM and PRKDC kinases.

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Meiosis involves DNA double-strand break (DSB) formation, recombination, and synapsis for genetic exchange.
  • ATM is a known regulator of these meiotic processes in mice.
  • The role of ATR, another DNA damage-regulated PIKK, in meiosis has been unclear due to challenges in germline-specific depletion.

Purpose of the Study:

  • To investigate the meiotic functions of the PIKK ATR in male mice.
  • To understand ATR's role in prophase I progression and germ cell survival.

Main Methods:

  • Germline-specific deletion of ATR in mice.
  • Analysis of chromosome structure, germ cell elimination, and synapsis.
  • Genetic analysis involving deletion of ATM and PRKDC.

Main Results:

  • ATR deletion causes chromosome axis fragmentation and germ cell elimination at mid pachynema.
  • This elimination is not rescued by ATM or PRKDC deletion, suggesting a PIKK-independent surveillance.
  • ATR is essential for synapsis, independent of DSB formation.
  • ATR regulates RAD51 and DMC1 loading to DSBs and recombination focus dynamics.

Conclusions:

  • ATR is a critical regulator of male mouse meiosis, impacting prophase I progression, chromosome integrity, and germ cell viability.
  • ATR's functions are genetically dissociable from DSB formation and involve regulating recombinase loading.
  • A PIKK-independent surveillance mechanism exists in the mammalian germline.

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