Papers by Stephen H Pilder
Dyneins, 2012
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Genetics
The effects of heterospecific combinations of mouse chromosome 17 on male fertility and transmiss... more The effects of heterospecific combinations of mouse chromosome 17 on male fertility and transmission ratio were investigated through a series of breeding studies. Animals were bred to carry complete chromosome 17 homologs, or portions thereof, from three different sources-Mus domesticus, Mus spretus and t haplotypes. These chromosome 17 combinations were analyzed for fertility within the context of a M. domesticus or M. spretus genetic background. Two new forms of hybrid sterility were identified. First, the heterospecific combination of M. spretus and t haplotype homologs leads to complete male sterility on both M. spretus and M. domesticus genetic backgrounds. This is an example of symmetrical hybrid sterility. Second, the presence of a single M. domesticus chromosome 17 homolog within a M. spretus background causes sterility, however, the same combination of chromosome 17 homologs does not cause sterility within the M. domesticus background. This is a case of asymmetrical hybrid ...
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Genetics, 1991
The effects of heterospecific combinations of mouse chromosome 17 on male fertility and transmiss... more The effects of heterospecific combinations of mouse chromosome 17 on male fertility and transmission ratio were investigated through a series of breeding studies. Animals were bred to carry complete chromosome 17 homologs, or portions thereof, from three different sources-Mus domesticus, Mus spretus and t haplotypes. These chromosome 17 combinations were analyzed for fertility within the context of a M. domesticus or M. spretus genetic background. Two new forms of hybrid sterility were identified. First, the heterospecific combination of M. spretus and t haplotype homologs leads to complete male sterility on both M. spretus and M. domesticus genetic backgrounds. This is an example of symmetrical hybrid sterility. Second, the presence of a single M. domesticus chromosome 17 homolog within a M. spretus background causes sterility, however, the same combination of chromosome 17 homologs does not cause sterility within the M. domesticus background. This is a case of asymmetrical hybrid ...
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Fertilization, 2002
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Proceedings of the National Academy of Sciences, 1986
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Mammalian Genome, 1997
ABSTRACT background were fertile [11]; and (B) no M. spretus/M, m. domesticus hybrid sterility ph... more ABSTRACT background were fertile [11]; and (B) no M. spretus/M, m. domesticus hybrid sterility phenotype mapped proximal to In4 [11]. Conclusion (A) was based on an examination of the fertility status of 16 M. m. domesticus males heterozygous for M. spretus and M. m. domesticus Chr 17 homologs [ 11 ]. Though 12 of the 16 males tested were fertile, the lineage(s) of the M. spretus Chr 17 homolog carried by the four sterile males was not investigated at the time. That lineage has since been traced as far back as possible, and results suggest that the M. spretus Chr 17 homolog carried by those four sterile males probably was not carried by the 12 fertile males. The presence of multiple M. spretus alleles at some loci was not totally unexpected, since the M. spretus animals used in the earlier studies were not inbred [11]. Subsequent breeding studies with the M. spretus Chr 17 homolog carried by the four sterile males (transmitted through females) have demonstrated that the male sterility phenotype breeds true: all M. m. domesticus males carrying this M. spretus Chr 17 homolog are sterile. Not surprisingly, SD 1 derives from this M. spretus Chr 17 homolog (and in turn, SD 2 from SD 1). Conclusion (B) was based on both the first conclusion and the fact that a majority of males beterozygous for M. spretus Chr 17 and the proximal part of a t haplotype (Inl, In2, and/or In3) were fertile, while all males heterozygous for M. spretus Chr 17 and the distal part of the t haplotype (In4) were sterile [11]. The fact that several males heterozygous for a M. spretus Chr 17 and the proximal part of the t haplotype were sterile was deemed of little significance at the time. As it turns out, this notion was mistaken. The Hst7S/Hst7 ' physiology of sterility differs significantly both quantitatively and qualitatively from that of Hst7S/Hst7 + (unpublished results). This, in addition to the fact that no known t hapiotype factor involved in homozygous t haplotype male sterility has been mapped to In2, suggests that Hst7 maps to Inl. If this hypothesis should be confirmed when more definitive recombinants become available, Hst7 could prove of benefit in characterizing S1, the t haplotype sterility factor previously mapped to Inl (Fig. 1) [15].
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Mammalian Genome, 1999
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Genetical Research, 1995
The t haplotypes are variant forms of the proximal one-third of chromosome 17 in the mouse. They ... more The t haplotypes are variant forms of the proximal one-third of chromosome 17 in the mouse. They contain four inversions (relative to the wildtype DNA) extending over most of this region and house a number of male sterility factors. Males carrying two complete t haplotypes (t/t) are sterile, as are males homozygous for S2, the sterility factor located in the most distal (relative to the centromere) inversion. Males homozygous for the sterility factor S1, located in the most proximal inversion, are not sterile; however, if such a male also is heterozygous for other sterility factors, then sterility results. It has been suggested therefore that homozygosity for S1 enhances the detrimental action of other sterility factors. Sperm from t/t males have severe motility defects and are unable to penetrate investment-free eggs, while sperm from fertile t/+ mice have less serious motility defects and exhibit a delay in penetration of investment-free eggs. To determine whether homozygosity for S1 enhances the cellular defects exhibited by sperm from mice heterozygous for other sterility factors, we compared the motility and egg-penetrating ability of sperm from fertile mice homozygous for S1 to that of sperm from mice carrying one complete t haplotype and one proximal or distal partial t haplotype. The data suggest that sperm from males carrying a proximal partial t haplotype and a complete t haplotype have serious defects in motility and penetration of the investment-free egg, and support the hypothesis that S1 enhances the detrimental effects of other sterility factors within the t haplotype.
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Developmental Biology, 1995
The t haplotypes, mutant forms of the proximal third of mouse chromosome 17 (the t complex), cont... more The t haplotypes, mutant forms of the proximal third of mouse chromosome 17 (the t complex), contain factors that contribute to defective sperm function in fertilization. Males carrying two t haplotypes (tx/ty mice) are sterile; their sperm have very poor motility and are unable to penetrate zona-free eggs. Although males carrying one t haplotype (t/+) are fertile, genetic evidence suggests that the sperm carrying the normal form of chromosome 17 (+t) are dysfunctional in fertilization, and some or all sperm have abnormal motility. Some of the same genetic factors that cause sterility in tx/ty males probably contribute to the dysfunction of +t sperm from t/+ males; however, it is unclear which steps in gamete interaction are defective in sperm from t/+ males, or whether the defects are similar to those observed in sperm from tx/ty males. We have developed a unique low sperm:egg ratio IVF assay for sperm function in fertilization. Using this assay, we have shown that tw5/+ sperm are less able than congenic +/+ sperm to penetrate the zona (probably due to their abnormal motility) and to penetrate the zona-free oocyte. Since tw5/tw32 sperm are unable to complete these same two steps in sperm-egg interaction, these specific deficits could be involved in both transmission ratio distortion and sterility. We have also shown that tw5/tw32 sperm are deficient in their ability to bind to the zona and to the oolemma. These results suggest that t haplotypes contain loci which affect a number of sperm functions and thus could be a rich source of genes important for sperm-egg interaction.
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Developmental Biology, 1993
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Biology of Reproduction, 1993
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Journal of Virology
The adenovirus 5 mutant H5dl337 lacks 146 base pairs within early region 1B. The deletion removes... more The adenovirus 5 mutant H5dl337 lacks 146 base pairs within early region 1B. The deletion removes a portion of the region encoding the E1B 21,000-molecular-weight (21K) polypeptide, but does not disturb the E1B-55K/17K coding region. The virus is slightly defective for growth in cultured HeLa cells, in which its final yield is reduced ca. 10-fold compared with wild-type virus. The mutant displays a striking phenotype in HeLa cells. The onset of cytopathic effect is dramatically accelerated, and both host cell and viral DNAs are extensively degraded late after infection. This defect has been described previously for a variety of adenovirus mutants and has been termed a cytocidal (cyt) phenotype. H5dl337 serves to map this defect to the loss of E1B-21K polypeptide function. In addition to its defect in the productive growth cycle, H5dl337 is unable to transform rat cells at normal efficiency.
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Molecular and cellular biology, 1986
The adenovirus type 5 mutant H5dl338 lacks 524 base pairs within early region 1B. The mutation re... more The adenovirus type 5 mutant H5dl338 lacks 524 base pairs within early region 1B. The mutation removed a portion of the region encoding the related E1B-55K and -17K polypeptides but did not disturb the E1B-21K coding region. The virus can be propagated in 293 cells which contain and express the adenovirus type 5 E1A and E1B regions, but it is defective for growth in HeLa cells, in which its final yield is reduced about 100-fold compared with the wild-type virus. The mutant also fails to transform rat cells at normal efficiency. The site of the dl338 defect was studied in HeLa cells. Early gene expression and DNA replication appeared normal. Late after infection, mRNAs coded by the major late transcription unit accumulated to reduced levels. At a time when transcription rates and steady-state nuclear RNA species were normal, the rate at which late mRNA accumulated in the cytoplasm was markedly reduced. Furthermore, in contrast to the case with the wild type, transport and accumulatio...
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Immunogenetics, 1989
We have characterized a novel mouse gene (D17Si11) on chromosome 17 that expresses a major transc... more We have characterized a novel mouse gene (D17Si11) on chromosome 17 that expresses a major transcript observed uniquely in the testes. TheD17Si11 locus has been mapped to the central region of chromosome 17 betweenH-2 andC3. Sequence analysis demonstrates several unusual features of this locus and its transcript: first is the presence of complementary sets of alternating purine and pyrmidine residues
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Immunogenetics, 1989
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Fertility and Sterility, 2005
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Cell
The mouse t complex responder (Tcr) locus plays a central haploid-specific role in the transmissi... more The mouse t complex responder (Tcr) locus plays a central haploid-specific role in the transmission ratio distortion phenotype expressed during germ cell differentiation in t-carrying males. The accumulated data map Tcr to a region of less than 500 kb. Over 400 kb of this region has been cloned and consists entirely of sequences associated with a clustered family of large cross-hybridizing elements of 30 kb to 70 kb in size. We have characterized a gene family within this region that is expressed uniquely in male germ cells with a complex pattern of RNA processing. Antibodies produced against a product of the putative open reading frame recognize a testes-specific polypeptide. Genetic data support the hypothesis that this polypeptide(s) functions to effect the Tcr phenotype.
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Journal of andrology
Hst7, a mouse hybrid sterility locus, has been mapped in close linkage to four other hybrid steri... more Hst7, a mouse hybrid sterility locus, has been mapped in close linkage to four other hybrid sterility loci, on proximal chromosome 17 within the t complex. When an allele (s) of Hst7 from the species Mus spretus is crossed into the Mus musculus domesticus (laboratory mouse) background, all male offspring are sterile. This occurs regardless of whether the Hst7 allele on the other chromosome 17 homolog is wild-type (+) or an allele (t) derived from the structurally variant homolog known as a t haplotype. Males of the Hst7 genotype s/+ produce sperm that, after release from the cauda epididymis, display moderate asthenospermia (straight line velocity = 49 +/- 4 microm/second, significantly lower than 102 +/- 7 microm/second for congenic wild-type controls) and normal morphology. However, males of the Hst7 genotype s/t produce sperm whose forward movement is below the detectable limit of the sperm motion analysis system. In addition, these sperm exhibit a variety of flagellar abnormalit...
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Nature, Jan 17, 1991
Mouse t haplotypes represent a variant form of chromosome 17 that has evolved the ability to prop... more Mouse t haplotypes represent a variant form of chromosome 17 that has evolved the ability to propagate through natural populations by the phenomenon of 'transmission ratio distortion' (TRD), in which heterozygous +/t males transmit their t-carrying chromosome to 95% or more of their offspring. Although multiple t-associated loci have a role in expression of this phenotype, only one--the t complex responder (Tcr) locus--is responsible for determining which of the two homologues of chromosome 17 will be transmitted at a high ratio. A candidate gene (Tcp-10b) for Tcr that is expressed in both meiotic and post-meiotic male germ cells has been cloned. But for this candidate gene to function as the haploid effector of TRD, the t-allele of this gene (Tcp-10bt) must express a unique product in a haploid-specific manner. Here we show that a change in the splicing pattern of Tcp-10bt transcripts occurs during sperm differentiation. This change results in a unique allele-specific and h...
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PLoS ONE, 2012
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Papers by Stephen H Pilder