In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 97, No. 20 ( 2000-09-26), p. 10814-10819
Abstract:
Two RecA homologs, Rad51 and Dmc1, assemble as cytologically
visible complexes (foci) at the same sites on meiotic chromosomes. Time course analysis confirms that co-foci appear and disappear as the
single predominant form. A large fraction of co-foci are eliminated in
a red1 mutant, which is expected as a characteristic of
the interhomolog-specific recombination pathway. Previous studies suggested that normal Dmc1 loading depends on Rad51. We show here that
a mutation in TID1 / RDH54 , encoding a RAD54 homolog, reduces Rad51-Dmc1 colocalization
relative to WT. A rad54 mutation, in contrast, has
relatively little effect on RecA homolog foci except when strains also contain a tid1 / rdh54 mutation. The role
of Tid1/Rdh54 in coordinating RecA homolog assembly may be very direct, because Tid1/Rdh54 is known to physically bind both Dmc1 and
Rad51. Also, Dmc1 foci appear early in a tid1 / rdh54 mutant. Thus, Tid1 may
normally act with Rad51 to promote ordered RecA homolog assembly by blocking Dmc1 until Rad51 is present. Finally, whereas double-staining
foci predominate in WT nuclei, a subset of nuclei with expanded chromatin exhibit individual Rad51 and Dmc1 foci side-by-side,
suggesting that a Rad51 homo-oligomer and a Dmc1 homo-oligomer assemble next to one another at the site of a single double-strand break (DSB)
recombination intermediate.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.97.20.10814
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
2000
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
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