PMID- 10318934
OWN - NLM
STAT- MEDLINE
DCOM- 19990617
LR  - 20190501
IS  - 0027-8424 (Print)
IS  - 0027-8424 (Linking)
VI  - 96
IP  - 10
DP  - 1999 May 11
TI  - Bloom's syndrome protein, BLM, colocalizes with replication protein A in meiotic 
      prophase nuclei of mammalian spermatocytes.
PG  - 5622-7
AB  - Bloom's syndrome (BS) is a rare autosomal recessive disorder of humans
      characterized by severe pre- and postnatal growth deficiency, immunodeficiency,
      genomic instability, and a predisposition to a wide variety of neoplasms. The
      genomic instability is evidenced in BS somatic cells as a high incidence of gaps 
      and breaks, chromatid exchanges, chromosome rearrangements, and locus-specific
      mutations. BS arises from a mutation in BLM, a gene encoding a protein with
      homology to the RecQ helicase family. Men with BS are sterile; women have reduced
      fertility and a shortened reproductive span. The current immunocytological study 
      on mouse spermatocytes shows that the BLM protein is first evident as discrete
      foci along the synaptonemal complexes (SCs) of homologously synapsed autosomal
      bivalents in late zygonema of meiotic prophase. BLM foci progressively dissociate
      from the synapsed autosomal axes during early pachynema and are no longer seen in
      mid-pachynema. BLM colocalizes with the single-stranded DNA binding replication
      protein A, which has been shown to be involved in meiotic synapsis. However,
      there is a temporal delay in the appearance of BLM protein along the SCs relative
      to replication protein A, suggesting that BLM is required for a late step in
      processing of a subset of genomic DNA involved in establishment of interhomologue
      interactions in early meiotic prophase. In late pachynema and into diplonema, BLM
      is more dispersed in the nucleoplasm, especially over the chromatin most
      intimately associated with the SCs, suggesting a possible involvement of BLM in
      resolution of interlocks in preparation for homologous chromosome disjunction
      during anaphase I.
FAU - Walpita, D
AU  - Walpita D
AD  - Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, 
      USA.
FAU - Plug, A W
AU  - Plug AW
FAU - Neff, N F
AU  - Neff NF
FAU - German, J
AU  - German J
FAU - Ashley, T
AU  - Ashley T
LA  - eng
GR  - CA50897/CA/NCI NIH HHS/United States
GR  - GM47797/GM/NIGMS NIH HHS/United States
GR  - GM55300/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (RPA1 protein, human)
RN  - 0 (Replication Protein A)
RN  - 0 (Rpa1 protein, mouse)
RN  - EC 3.6.1.- (Adenosine Triphosphatases)
RN  - EC 3.6.1.- (Bloom syndrome protein)
RN  - EC 3.6.4.- (DNA Helicases)
RN  - EC 3.6.4.12 (RecQ Helicases)
SB  - IM
MH  - Adenosine Triphosphatases/analysis/*metabolism
MH  - Animals
MH  - DNA Helicases/analysis/*metabolism
MH  - DNA Replication
MH  - DNA-Binding Proteins/analysis/*metabolism
MH  - Humans
MH  - Image Processing, Computer-Assisted
MH  - Male
MH  - Mice
MH  - Microscopy, Fluorescence
MH  - Prophase
MH  - RecQ Helicases
MH  - Recombination, Genetic
MH  - Replication Protein A
MH  - Spermatocytes/*metabolism
MH  - Synaptonemal Complex/genetics
PMC - PMC21910
EDAT- 1999/05/13 00:00
MHDA- 1999/05/13 00:01
CRDT- 1999/05/13 00:00
PHST- 1999/05/13 00:00 [pubmed]
PHST- 1999/05/13 00:01 [medline]
PHST- 1999/05/13 00:00 [entrez]
AID - 10.1073/pnas.96.10.5622 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1999 May 11;96(10):5622-7. doi:
      10.1073/pnas.96.10.5622.