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From the * Department of Pathology and Laboratory
Medicine and
Department of Molecular Biology,
Cell Biology and Biochemistry, Brown University, Providence, RI
| Correspondence to: Jan Klysik, Brown University, Department of Molecular Biology Cell Biology and Biochemistry, Division of Biology and Medicine, 70 Ship St, Providence, RI 02912 (e-mail: Jan_Klysik{at}Brown.edu). |
B), and G protein coupled receptor
(GPCR) signaling cascades and is implicated as a factor in numerous
physiological processes and disease states including metastasis. Testicular
germ cells also express high levels of RKIP mRNA during spermatogenesis,
particularly from late pachytene spermatocytes through step 15 elongate
spermatids. Therefore, the sensitivity of spermatogenesis to injury was
compared in wild-type and RKIP-1-/- mice. Unlike what has been
described with tumor suppressors such as p53, RKIP-1-/- and
wild-type mice were equally sensitive to germ cell toxicity by x-irradiation
as assessed by terminal deoxynucleotidyl transferase biotin-deoxyuridine
triphosphate (dUTP) nick end labeling (TUNEL) positivity 9 hours after a 5 Gy
exposure and testicular spermatid head counts 15.5 days after 0.5 Gy exposure.
Recent findings also indicate that RKIP is a decapacitation factor receptor on
sperm. The present study demonstrates that sperm from RKIP-deficient mice are
precociously capacitated compared with their wild-type counterparts. Data from
mating experiments indicate decreased reproduction rates between crosses of
RKIP-1-/- male mice and either heterozygous or RKIP-1-/-
females. Furthermore, RKIP immunolocalization of epididymal sperm supports
transfer of the protein from germ cell cytoplasm to the sperm via the
cytoplasmic droplet during epididymal transport. Overall, these studies
indicate an important role for RKIP in reproduction as a modulator of
capacitation but not in the regulation of testicular injury.
Key words: PEBP, testis
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