The ATR (ataxia telangiectasia- and RAD3-related) protein is present on mei
otic prophase chromosome cores and paired cores (synaptonemal complexes, SC
s). Its striking characteristic is that the protein forms dense aggregates
on the cores and SCs of the last chromosomes to pair at the zygotene-pachyt
ene transition. It would appear that the ATR protein either signals delays
in pairing or it is directly involved in the completion of the pairing phas
e. Atm-deficient spermatocytes, which are defective in the chromosome pairi
ng phase, accumulate large amounts of ATR. The behaviour of ATR at meiotic
prophase sets it apart from the distribution of the RAD51/DMC1 recombinase
complex and our electron microscope observations confirm that they do not c
o-localize. We failed to detect ATM in association with cores/SCs and we ha
ve reported elsewhere that RAD1 protein does not co-localize with DMC1 foci
. The expectation that putative DNA-damage checkpoint proteins, ATR, ATM an
d RAD1, are associated with RAD51/DMC1 recombination sites where DNA breaks
are expected to be present, is therefore not supported by our observations
.