The long term objective of this study is to determine what extragenetic contribution the mammalian spermatozoan provides the ovum. Using microinjection techniques, sperm components will be injected into mouse ova that have been parthenogenically activated. Special attention will be given to the midpiece-tail component of the spermatozoan to determine the possible contribution and fate of the paternal mitochondria. Although the inheritance of mitochondria appears to be solely maternal, in vertebrates the mitochondria of the spermatozoa enter the egg at fertilization and are detectable during early embryogenesis. To evaluate whether the molecular basis for maternal inheritance of mitochondria can be a preprogrammed deficiency of the male mitochondrial genome, the DNA sequence of several regulatory regions of the mitochondiral DNA from sperm and ova will be compared. These studies will help identify epigenetic and nuclear regulated processes that are essential for normal mammalian development. A better understanding of these events is necessary to explain how pertubations lead to birth defects. In addition a more detailed comprehension of the biochemical events at and following fertilization will provide necessary information to aid in the treatment of the infertile and may provide superior approaches to fertility control.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD011878-08
Application #
3311696
Study Section
Reproductive Biology Study Section (REB)
Project Start
1979-09-30
Project End
1988-08-31
Budget Start
1986-09-01
Budget End
1987-08-31
Support Year
8
Fiscal Year
1986
Total Cost
Indirect Cost
Name
Tufts University
Department
Type
Schools of Arts and Sciences
DUNS #
073134835
City
Medford
State
MA
Country
United States
Zip Code
02155
Syed, V; Hecht, N B (2002) Disruption of germ cell-Sertoli cell interactions leads to spermatogenic defects. Mol Cell Endocrinol 186:155-7
Syed, V; Hecht, N B (2001) Selective loss of Sertoli cell and germ cell function leads to a disruption in sertoli cell-germ cell communication during aging in the Brown Norway rat. Biol Reprod 64:107-12
Chennathukuzhi, V M; Lefrancois, S; Morales, C R et al. (2001) Elevated levels of the polyadenylation factor CstF 64 enhance formation of the 1kB Testis brain RNA-binding protein (TB-RBP) mRNA in male germ cells. Mol Reprod Dev 58:460-9
Syed, V; Gomez, E; Hecht, N B (1999) mRNAs encoding a von Ebner's-like protein and the Huntington disease protein are induced in rat male germ cells by Sertoli cells. J Biol Chem 274:10737-42
Syed, V; Gomez, E; Hecht, N B (1999) Messenger ribonucleic acids encoding a serotonin receptor and a novel gene are induced in Sertoli cells by a secreted factor(s) from male rat meiotic germ cells. Endocrinology 140:5754-60
Syed, V; Hecht, N B (1998) Rat pachytene spermatocytes down-regulate a polo-like kinase and up-regulate a thiol-specific antioxidant protein, whereas sertoli cells down-regulate a phosphodiesterase and up-regulate an oxidative stress protein after exposure to methoxyethanol and met Endocrinology 139:3503-11
Gu, W; Hecht, N B (1997) The enzymatic activity of Cu/Zn superoxide dismutase does not fluctuate in mouse spermatogenic cells despite mRNA changes. Exp Cell Res 232:371-5
Yiu, G K; Murray, M T; Hecht, N B (1997) Deoxyribonucleic acid-protein interactions associated with transcriptional initiation of the mouse testis-specific cytochrome c gene. Biol Reprod 56:1439-49
Yiu, G K; Hecht, N B (1997) Novel testis-specific protein-DNA interactions activate transcription of the mouse protamine 2 gene during spermatogenesis. J Biol Chem 272:26926-33
Choi, Y C; Aizawa, A; Hecht, N B (1997) Genomic analysis of the mouse protamine 1, protamine 2, and transition protein 2 gene cluster reveals hypermethylation in expressing cells. Mamm Genome 8:317-23

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