[Contraception and voluntary sterilization: male sterilization and the possibility of reversal].
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Contraception↗
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Results for “STERILITY, MALE”
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Induction of male sterility through manipulation of genetic mechanisms present in vector species of Chagas disease. (Remarks on integrating sterile-male release with insecticidal control measures against vectors of Chagas disease).
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Animals↗
Translocation of adenine nucleotides in the mitochondria of male sterile and male fertile sorghum.
The translocation of ATP from the inside to the outside of the mitochondrial membrane has been studied in a male sterile (2219 A) and a male fertile (2219 B) line of sorghum. The translocation of ATP was found to be substantially lower in case of mitochondria from the male sterile line. The affinity of adenine nucleotides to the translocator proteins of the mitochondrial membrane was found to be almost one half in case of 2219 A as compared to 2219 B when the Km for ATP-ADP was determined by two different assays. It is proposed that the inadequate supply of ATP in the cytosol resulting from its inefficient translocation may contribute to the male sterility in this line.
Adenine Nucleotides↗
Organizational differences between cytoplasmic male sterile and male fertile Brassica mitochondrial genomes are confined to a single transposed locus.
Comparison of the physical maps of male fertile (cam) and male sterile (pol) mitochondrial genomes of Brassica napus indicates that structural differences between the two mtDNAs are confined to a region immediately upstream of the atp6 gene. Relative to cam mtDNA, pol mtDNA possesses a 4.5 kb segment at this locus that includes a chimeric gene that is cotranscribed with atp6 and lacks an approximately 1kb region located upstream of the cam atp6 gene. The 4.5 kb pol segment is present and similarly organized in the mitochondrial genome of the common nap B.napus cytoplasm; however, the nap and pol DNA regions flanking this segment are different and the nap sequences are not expressed. The 4.5 kb CMS-associated pol segment has thus apparently undergone transposition during the evolution of the nap and pol cytoplasms and has been lost in the cam genome subsequent to the pol-cam divergence. This 4.5 kb segment comprises the single DNA region that is expressed differently in fertile, pol CMS and fertility restored pol cytoplasm plants. The finding that this locus is part of the single mtDNA region organized differently in the fertile and male sterile mitochondrial genomes provides strong support for the view that it specifies the pol CMS trait.
Adenosine Triphosphatases↗
New frontiers in the treatment of male sterility.
Male factor responsibility in couple infertility has been exponentially increasing in recent years, due both to improved diagnostic techniques and to the important role of lesive factors, mainly environmental, on reproductive male function. Therefore, male infertility therapy is one of the most challenging topics of modern clinical medicine. Unfortunately, however, 30% of cases of male infertility must still be classified as "idiopathic." In these cases, no "causal" treatments can be used but only empiric treatments. These are lacking of an etiopathogenetic basis, and often result from theoretical concepts without a proven statistical effectiveness. These facts have somehow allowed the explosive development of the assisted reproduction techniques (ART). Andrologist's therapeutic strategies have so changed and are no longer aimed, as in the past, to achieve an increase in the spermatozoa number, but rather to improve the "quality" of semen, that is, the "fertility potential."
Bacterial Infections↗
Male-sterility of thermosensitive genic male-sterile rice is associated with premature programmed cell death of the tapetum.
The tapetum plays a crucial role in pollen development. This secretory tissue produces numerous nutritive proteins necessary for pollen maturation. The tapetum, whose cells undergo programmed cell death (PCD), is completely diminished by the time the pollen is fully mature. Our previous studies on a thermosensitive genic male-sterile (TGMS) rice (Oryza sativa L.) suggested that male-sterility was due to failure in pollen development. In this paper we describe how further analysis of the TGMS rice revealed that male-sterility is associated with premature PCD of the tapetum. Cytological observations of TGMS rice anthers at various developmental stages indicated that PCD initiates at an early stage of pollen development and continues until the tapetal cells are completely degraded, resulting in pollen collapse. Transmission electron microscopy showed the morphologically distinct hallmarks of apoptosis, including cytoplasmic shrinkage, membrane blebbing, and vacuolation. Identification of DNA fragmentation using the TUNEL assay supports the hypothesis that premature PCD is associated with male-sterility in the rice. The tissue-specific feature of the thermosensitive genic male-sterile phenotype is discussed with regard to PCD during anther development.
Apoptosis↗
Meiotic studies of translocations causing male sterility in the mouse. II. Double heterozygotes for Robertsonian translocations.
Unusual meiotic behavior of the XY chromosome pair was observed in sterile male mice doubly heterozygous for two Robertsonian translocations, Rb(16.17)7Bnr and Rb(8.17)1Iem. Nonrandom association between the X chromosome and the translocation configuration, ascertained from the frequencies of relevant C-band contacts, was found in 9 of 10 sterile males. Besides the nonrandom association, the XY chromosomes showed signs of impaired condensation, as judged by measurement of their lengths at diakinesis/MI of the first meiotic division. In contrast, neither nonrandom contact nor decondensation of the XY chromosomes pair was found in fertile males heterozygous for a single Robertsonian translocation, Rb1Iem or Rb7Bnr. The present observations lend indirect support to the working hypothesis advanced previously, the assumption that interference with X-chromosome inactivation is a possible cause of spermatogenic breakdown in carriers of various male-sterile chromosomal transloations. Alternative explanations of the available data, which cannot be ruled out, are briefly discussed.
Animals↗
The role of X-linked lethal and viable male-sterile mutations in male gametogenesis of Drosophila melanogaster: genetic analysis.
The possibility that viable male-sterile mutations occur in vital genes and the role played by lethal mutations and viable male-steriles in male gametogenesis were studied. Five sterile loci were identified among the 30 most proximal vital loci of the X-chromosome and two of them were shown to be allelic with lethal mutations. Fertility test on gynanders for nonautonomous lethal mutations proved that vital genes operate autonomously in male gonads, independently of their effect on somatic tissues. Fertility tests of ts lethals, shifted to the nonpermissive temperature after the TSP, showed that 40% of vital genes function in male gonads. It is further shown that about the same proportion of vital genes is operating in female gonads and that the two groups overlap by about 70%. The role of viable and lethal male gametogenesis is discussed in detail.
Drosophila melanogaster↗
Anopheles stephensi: effect of gamma-radiation and chemosterilants on the fertility and fitness of males for sterile male releases.
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Animals↗
Transgene insertion induced dominant male sterility and rescue of male fertility using round spermatid injection.
Transgene insertions in the mouse often cause mutations at chromosomal loci. Analysis of insertion mutations that cause male sterility may lead to the identification of novel molecular mechanisms implicated in male fertility. Here we show a line of transgenic mice with dominant inheritance of male sterility (DMS) that was found amid several lines that were normally fertile. Transgene-positive males from this line invariably were sterile, whereas transgenic females and transgene-negative male littermates were fertile. Histologic analysis and TUNEL staining for apoptotic cells in DMS testis showed spermatogenesis arrest at metaphase of meiosis I (M-I), accompanied by massive apoptosis of spermatocytes. Meiosis I arrest was incomplete, however, as small numbers of spermatids and spermatozoa were found. Both round spermatids and spermatozoa were evaluated for their permissiveness in the assisted reproductive technologies intracytoplasmic sperm injection (ICSI) and round spermatid injection (ROSI). Surprisingly, ROSI but not ICSI gave live offspring, suggesting that mature sperm had deteriorated by the time of recovery from the epididymis. Mapping the transgene insertion by fluorescence in situ hybridization revealed a site on chromosome 14 D3-E1. Two candidate genes, GFR alpha 2 and GnRH, that were previously mapped to that region and the functions of which in spermatogenesis are well established were not altered in DMS. As a consequence, positional cloning of the DMS locus will be essential to identify new molecules potentially involved in arrest at M-I. Furthermore, mice carrying this genetic trait might be useful for studies of assisted reproductive technologies and male contraceptives.
Animals↗
Ogura cytoplasmic male-sterility (CMS)-associated orf138 is translated into a mitochondrial membrane polypeptide in male-sterile Brassica cybrids.
Transcription of a putative mitochondrial gene (orf138) has previously been correlated with Ogura cytoplasmic male-sterility (CMS) in rapeseed cybrids. In this paper, studies performed on a Brassica cybrid with a different organization of the orf138 locus confirm this association. We also show that mitochondria isolated from male-sterile rapeseed plants synthesize a polypeptide of 19 kDa, which is absent in fertile revertants. Antibodies against a glutathione S-transferase-ORF138 fusion protein were raised to establish that this 19 kDa polypeptide is the product of orf138. The anti-ORF138 serum was used to demonstrate that the orf138 translation product occurs only in sterile cybrids and co-purifies with the mitochondrial membrane fraction.
Blotting, Western↗
[The role of prolactin in the pathogenesis of male sterility].
To study the causal relationship between the hormonal status and spermatographic data in sterile males, the authors investigated the correlations between the plasma levels of testosterone, estradiol, prolactin and gonadotrophin and certain parameters of spermograms and computed the correlative relationship of those values. The findings demonstrated the increased levels of prolactin (249.09 +/- 39.6 mu/U/ml), significantly exceeding the normal (132.6 +/- 32.4 mu/U/ml), a tendency towards a decrease in the levels of FSH and testosterone (up to 7.01 +/- 0.70 nmol/l versus 12.57 +/- 0.39 nmol/l in health) and manifest elevation of estradiol levels (up to 634.71 +/- 29.16 nmol/l versus 205.02 +/- 18.60 nmol/l), as well as its ratio to the testosterone levels. The number of spermatozoa in 1 ml was found decreased up to 29.6 +/- 4.10 million, the volume of ejaculate was reduced to 2.7 +/- 0.41 ml, while the percentage of immobile spermatozoa rose to 40.00 +/- 4.76. Despite of some pathological changes evidenced by spermograms, there was the only parameter--the volume of ejaculate--that was directly dependent on the levels of prolactin, their correlation was reversed. Decreased numbers of spermatozoa and their motility were not related to hyperprolactinemia. Moreover, there was a positive correlation between the levels of prolactin and the motility of spermatozoa in sterile patients. Therefore, decreased number and motility of spermatozoa turned to be dependent not on prolactin but sex hormone levels. However, ejaculation was found unfeasible in male with high levels of hyperprolactinemia.
Adult↗
The nucleo-mitochondrial conflict in cytoplasmic male sterilities revisited.
Cytoplasmic male sterility (CMS) in plants is a classical example of genomic conflict, opposing maternally-inherited cytoplasmic genes (mitochondrial genes in most cases), which induce male sterility, and nuclear genes, which restore male fertility. In natural populations, this type of sex control leads to gynodioecy, that is, the co-occurrence of female and hermaphroditic individuals within a population. According to theoretical models, two conditions may maintain male sterility in a natural population: (1) female advantage (female plants are reproductively more successful than hermaphrodites on account of their global seed production); (2) the counter-selection of nuclear fertility restorers when the corresponding male-sterility-inducing cytoplasm is lacking. In this review, we re-examine the model of nuclear-mitochondrial conflict in the light of recent experimental results from naturally occurring CMS, alloplasmic CMS (appearing after interspecific crosses resulting from the association of nuclear and cytoplasmic genomes from different species), and CMS plants obtained in the laboratory and carrying mitochondrial mutations. We raise new hypotheses and discuss experimental models that would take physiological interactions between cytoplasmic and nuclear genomes into account.
DNA, Mitochondrial↗
Premature dissolution of the microsporocyte callose wall causes male sterility in transgenic tobacco.
Male sterility in a petunia cytoplasmic male sterile line has been attributed to the early appearance of active callase, a beta-1,3-glucanase, in the anther locule. This leads to premature dissolution of the callose walls surrounding the microsporogenous cells. We have mimicked this aspect of the petunia line in transgenic tobacco by engineering the secretion of a modified pathogenesis-related vacuolar beta-1,3-glucanase from the tapetum prior to the appearance of callase activity in the locule. Plants expressing the modified glucanase from tapetum-specific promoters exhibited reduced male fertility, ranging from complete to partial male sterility. Callose appearance and distribution are normal in the male sterile transgenic plants up to prophase I, whereupon callose is prematurely degraded. Meiosis and cell division occur normally. The resultant microspores have an abnormally thin cell wall that lacks sculpturing. The tapetum shows hypertrophy. Male sterility is probably caused by bursting of the aberrant microspores at a time corresponding to microspore release. These results demonstrate that premature callose degradation is sufficient to cause male sterility and suggest that callose is essential for the formation of a normal microspore cell wall.
Base Sequence↗
[On the surgical treatment of male sterility. (On the supplementary operations of various complications of male sterility)].
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Humans↗
Specific expression in reproductive tissues and fate of a mitochondrial sterility-associated protein in cytoplasmic male-sterile bean.
In common bean, cytoplasmic male sterility has been associated with a unique sequence found in the mitochondrial genome, designated pvs (for Phaseolus vulgaris sterility sequence). Within the pvs sequence, two open reading frames are encoded, ORF98 and ORF239. We have raised rabbit polyclonal antibodies against Pvs-ORF239 to evaluate the role of this putative male sterility-associated protein. Histological investigation of pollen development revealed that in the male-sterile bean line, callose deposition was abnormal and microspores remained as tetrads as previously reported. Pvs-ORF239 was found to be localized within the reproductive tissues of the male-sterile bean line, in contrast to all other cytoplasmic male sterility systems studied to date. This protein was associated with mitochondria, the callose layer, and developing primary cell walls during microsporogenesis. Expression of pvs-orf239 was not detected in fertile plants containing restorer gene Fr2. These observations, together with previous reports, suggest that nuclear restorer gene Fr2 interferes with expression of the pvs region post-transcriptionally.
Animals↗
Molecular diversity of male sterility inducing and male-fertile cytoplasms in the genus Helianthus.
The organisation of mtDNA was investigated for 28 sources of cytoplasmic male sterility (CMS) and a fertile line (normal cytoplasm) of Helianthus annuus by Southern hybridisation. In addition to nine known mitochondrial genes ( atp6, atp9, cob, coxI, coxII, coxIII, 18S, 5S and nd5) three probes for the open reading frames in the rearranged area of PET1, orfH522, orfH708 and orfH873, were used. Genetic similarities of the investigat-ed cytoplasms varied between 0.3 and 1. Cluster analyses using the UPGMA method allowed the distinction of ten mitochondrial (mt) types between the 29 investigated cytoplasms. Most mitochondrial types comprise two or more CMS sources, which could not be further separated, like the PET1-like CMS sources (with the exception of ANO1 and PRR1), or ANN1/ANN2/ANN3, ANN4/ ANN5, ARG3/RIG1, BOL1/EXI1/PEF1/PEP1 and GIG1/ PET2. ANL1, ANL2 and the fertile cytoplasms are also regarded as one mitochondrial type. Unique banding patterns were only observed for ANT1 ( atp6), MAX1 ( atp6, orfH522 and orfH708) and PRR1 ( coxII). However, four of the mitochondrial types showed unique hybridisation signals: ANN4/ANN5 had characteristic bands for atp6 and orfH708, PEF1/PEP1/EXI1/BOL1 for atp6and coxII, and PET2/GIG1 for atp9. The PET1-like cytoplasms all shared the same patterns for orfH522, orfH708and cob (except ANO1). It could be demonstrated that CMS sources, like, e.g., PET2 and PEF1, are different from PET1 in mtDNA organisation and the CMS mechanism. Therefore, these CMS sources represent interesting candidates for the development of new hybrid breeding systems based on new CMS mechanisms.
Journal Article↗
[Male sterility. Experience of an andrologist].
Male sterility is taken as a paradigm for a new approach to andrology. Although known about since Antiquity, responsibility of man in conjugal sterility has only been recognized in the last half century. All the same, even to day, it is not always accepted: although apparently obsolete since women's sexual liberation, this denial often manifests itself in patients behaviour, as well as in their doctor's. Until now, as far as we know, no andrologist has taken into account this strange denial. The aim of this paper is to draw attention to the need for the andrologist to be aware of it in his approach to the sterile man. History of male sterility emphasizes the coexistence, since Antiquity, of two opposite preoccupations, those of doctors thoughtful of proving male sterility existence and those of philosophers, often determined to deny it. Steps of knowledge as well as social structures institutionalizing its dissembling are described. Sexual liberation which claimed to put and end to women's dependence on men is often illusory; acceptance of equality of sexes by men is often more apparent that real. At present, the medicalization of male sterility leads some patients and even some doctors to an activist behaviour which demonstrate their inability to accept even the concept of man sterility. In our opinion, to be an andrologist in the full sense of the word means not only to know the biology of reproduction and the progresses of research in this domain, but also and mainly to be aware of the permanence of prejudices and fantasies infallibly conveyed by the idea of sterility in every one, andrologist included.(ABSTRACT TRUNCATED AT 250 WORDS)
Humans↗