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Results for “male sterility”

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At least 19 recordsLinked to original sources
PubMed1979

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↗
PubMed1978

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↗
PubMed2025

Alternative splice acceptor site in MSH4 gene is responsible for male sterility conferred by ms5 in soybean.

In soybean breeding, using the recessive male-sterile ms5 gene, derived from fast neutron mutagenesis, for recurrent selection is advantageous because of the d2 locus, which controls cotyledon color in mature seeds and can be used as a phenotypic selection marker for ms5 male sterility. However, occasional self-fertilization occurs because of the elimination of d2 linkage and instability of male sterility. Elucidating the mechanism and the gene responsible for ms5 male sterility may resolve these problems. Using fine mapping with 15 simple sequence repeat (SSR) markers, we narrowed down the candidate ms5 locus to a 54-kbp region. Bulked-DNA analysis using next-generation sequencing revealed a deletion as a candidate variation in the region. This 15-bp deletion and a nucleotide substitution were identified in intron 1 of MutS homolog (GmMSH4), which modulates chromosomal recombination in meiosis. The ms5 transcript contained a novel exon with a premature termination codon. This exon originated from an alternative splice acceptor site caused by the deletion and nucleotide substitution, disrupting gene function. Co-segregation of male sterility with five independent mutations in GmMSH4 was confirmed using progeny of mutant lines. Mutations in GmMSH4 led to biased DNA partitioning during meiosis, resulting in collapsed or enlarged pollen and suggesting that ms5 male sterility is caused by the failure of pollen formation during meiosis due to the loss of function of GmMSH4. These findings could help explain the mechanism of instability of ms5 male sterility and improve the efficiency of recurrent selection using DNA markers in soybean breeding.

Glycine max↗
PubMed1977

Meiotic studies of translocations causing male sterility in the mouse. I. Autosomal reciprocal translocations.

A new meiotic phenomenon is described in male heterozygous for the male-sterile translocations T(10;13)199H, T(16;17)43H, and T(7;19)145H. The phenomenon consists of a nonrandom contact between the C bands of the X chromosome and the translocation configuration in diakinesis/metaphase I plates. Translocation configurations with positively heteropycnotic regions, oftern associated with the allocyclic X chromosome, are found in some early diakineses that have not been overtreated with alkali. Such heteropycnosis of a part of translocated autosome, apparently in phase with the allocyclic X, is typical for all three male-sterile translocations. In contrast to these findings, neither nonrandom contacts nor positive heteropycnosis of the translocation configuration can be found in males heterozygous for the translocation T(9;17)138Ca, which does not impair spermatogenesis. Dissociation of the X and Y at diakinesis is significantly enhanced in sterile males, though the occurrence of dissociation is evidently not related to the presence of the C-band contact between translocated chromosomes and the X. A working hypothesis is proposed, relating the observed nonrandom C-band contact and heteropycnosis of translocated chromosomes to a presumed impairment of X inactivation in primary spermatocytes and to consequent failure of spermatogenesis. An alternative explanation cannot be excluded, however, which would account for the hitherto available data wihtout postulating any causal relationship between the meiotic findings and male sterility. Both alternatives are amenable to experimental verification.

Animals↗
PubMed1979

Hybrid dysgenesis in Drosophila melanogaster: the biology of female and male sterility.

High levels of female and male sterility were observed among the hybrids from one of the two reciprocal crosses between a wild strain of D. melanogaster known as pi2 and laboratory strains. The sterility, which is part of a common syndrome called hybrid dysgenesis, was found to be associated with the rudimentary condition of one or both of the ovaries or testes. All other tissues, including those of the reproductive system were normal, as were longevity and mating behavior. The morphological details of the sterility closely mimic the agametic condition occurring when germ cells are destroyed by irradiation or by the maternal-effect mutation, grandchildless. We suggest that sterility in hybrid dysgenesis is also caused by failure in the early development of germ cells. There is a thermo-sensitive period beginning at approximately the time of initiation of mitosis among primordial germ cells a few hours before the egg hatches and ending during the early larval stages. Our results suggest that hybrid dysgenesis, which also includes male recombination, mutation and other traits, may be limited to the germ line, and that each of the primordial germ cells develops, or fails to develop, independently of the others. This hypothesis is consistent with the observed frequencies of unilateral and bilateral sterility, with the shape of the thermosensitivity curves and with the fact that males are less often sterile than females. The features of this intraspecific hybrid sterility are found to resemble those seen in some interspecific Drosophila hybrids, especially those from the cross D. melanogaster X D. simulans.

Animals↗
PubMed1979

Electrophoretic analyses of lactate dehydrogenase C4 in testes and vesicular glands of normal and male sterile translocation mice.

Lactate dehydrogenase (LDH) C, activity was observed in testis extracts from normal mice but was progressively reduced in mice carrying the male-sterile translocations T31H, T32H, T37H, T38H, T40H and T42H, with no detectable activity being observed in the last two mice. None of the vesicular gland extracts from these male-steriles showed LDH-C4 activity, unlike normal mice. The differential LDH-C4 activity in male-sterile testes is interpreted as reflecting the varying stages of the spermatogenic defect during meiosis. In general, early meiotic defects exhibited no LDH-C4 activity whereas late stage (usually after metaphase-1 stage) defect animals exhibited some activity. The results also provide evidence for contaminating sperm being the source of normal vesicular gland LDH-C4 activity.

Animals↗
PubMed1976

[Impotence and male sterility].

The causes of sexual impotence, including disturbances of ejaculation, and the methods of treatment are described. In the vast majority of cases male sterility results from a disorder of spermatogenesis. The main factors responsible for infertile semen are discussed: in most cases the causes are unknown. It is to be hoped that progress in research into human reproduction and recent diagnostic advances will provide the groundwork for more successful therapy of male sterility.

Chromosome Aberrations↗
PubMed1977

Possible mitochondrial involvement in mechanism of cytoplasmic male sterility in maize (Zea mays L.).

The mechanism of cytoplasmic male sterility was investigated in maize by isolating mitochondria from seedlings and various anther stages and analyzing cytochrome oxidase and succinic dehydrogenase biochemically and electrophoretically. Sterile anthers exhibited a lack of biochemical activity and fewer isozymatic bands for cytochrome oxidase. No apparent differences were detected biochemically or electrophoretically between fertile and sterile anthers for succinate dehydrogenase.

Electron Transport Complex IV↗
PubMed2025

Advances in Cytoplasmic Male Sterility in Sugar Beet from Mitochondrial Genome Structural Dynamics and Nuclear-Cytoplasmic Coordination.

Sugar beet (Beta vulgaris L.) is a globally important sugar crop whose hybrid breeding system relies heavily on cytoplasmic male sterility (CMS) lines. Recent advances in sugar beet genomics, particularly the release of high-quality reference genomes and the characterization of organellar genomes, have provided a foundation for elucidating the molecular genetic mechanisms of CMS. Furthermore, innovations in gene editing technologies are enabling transformative functional studies in this field. The precise targeting of CMS-associated mitochondrial genes and nuclear restorer-of-fertility genes not only allows for direct investigation of theoretical models governing fertility regulation through nuclear-cytoplasmic interactions but also holds promise for the targeted development of sterile and restorer lines. This review systematically summarizes progresses in sugar beet genomics, the development of gene editing tools, and the current understanding of the molecular genetics of CMS and fertility restoration in sugar beet. Although challenges remain-such as efficient delivery of editing tools into mitochondria and coordinated editing of multiple genes-the integration of genomic and gene editing technologies is expected to accelerate multi-omics-guided dissection of CMS mechanisms. These advances will facilitate the precise design of high-yield, high-sugar, and stress-resistant sugar beet hybrids, thereby providing core scientific and technological support for the sustainable development of the global sugar industry.

Beta vulgaris↗
PubMed1979

Male sterility associated with familial translocation heterozygosity: t(8;15) (q22;p11).

During the investigation of the family of a subject consulting for primary sterility, the same oligoteratospermia was found in two of his brothers. The three karyotypes of these subjects exhibited an equilibrated reciprocal autosomal translocation t(8;15) (q22;p11), which was also detected in their mother. The karyotypes of the remaining siblings, one brother and one sister, were normal. The semen analysis of the sterile subjects suggests that the block of gamete production occurs at the beginning of spermiogenesis. The chromosomal anomaly, which has no effect on the reproduction of the mother, leads to sterility of the male offspring bearing it.

Adult↗
PubMed1977

Spermatogenesis revisited. IV. Abnormal spermiogenesis in mice homozygous for another male-sterility-inducing mutation, hpy (hydrocephalic-polydactyl).

Gametogenesis is normal through meiosis and the earliest phases of spermiogenesis in male-sterile mice homozygous for the recessive, pleiotropic, mutation hpy (hydrocephalic-polydactyl). However, structurally complete sperm flagella were not encountered. Instead partially assembled axonemal structures and/or poorly organized aggregates of other tail components (mitochondria, outer coarse fibers) were seen at the posterior poles of nuclei in older spermatids. The ultrastructure of centrioles in spermatids was normal, but that of axonemes associated with them was not. These findings suggest that the observed flagella dysgenesis results from defects in assembly rather than from defective intiation centers. Released "gameters" usually consisted of ditorted nuclei and associated acrosome enclosed in a relatively close fitting plasma membrane. Perturbations of sperm head development were also encountered; they included extreme nuclear elongation, and distortion of the acrosome and underlying nuclear material by impushings of finger-like processes of Sertoli cells. It is believed that sperm head anomalies are secondary consequences of the mutant condition. The findings support the view that the hpy locus represents one of a number of genes primarily involved in the mediation of flagella development.

Acrosome↗
PubMed1976

[Attempt at a standardized interpretation of testicular histopathology in male sterility].

The authors present a standard for interpreting the histopathology of testicular biopsies carried out during the framework of investigation of male sterility. The standard is based on a study of the alterations in the seminiferous tubes (T), the peritubular membranes (M) and the interstitial tissue (I). This method of histological assessment has been used to study 35 subjects on whom bilateral bipolar biopsies were carried out (130 specimens). The statistical study showed: a) the absence of any difference between the pieces taken from the two poles in each testis; b) the level of concentration of spermatozoa could not be tied up with any of the three histological parameters. This applied also for hormone levels with the exception of GUT which seem to correlate directly with M; c) the presence of a varicocoele does not reflect in any way the membrane or the interstitial tissue; d) spermograms carried out after the biopsies showed that testicular biopsy does not cause permanent trauma to the testis. The advantages and disadvantages of this quantitative method are discussed.

Adult↗
PubMed1977

[Analysis of 830 case histories of male sterility of which 282 are usable. Results of our diagnostic investigations and therapeutic procedures].

Overall results are given of the investigation and treatment of 282 cases of male sterility: 245 cases of secretory and 37 of excretory sterility; 126 cases in which treatment produced no change, 110 cases showing biological improvement and 45 cases in which pregnancy occurred; 128 of the 282 men had varicoceles. There were three groups of patients; 1) Those with azoospermia: 59 cases, predominantly with excretory problems, bilateral atrophy and chromosomal anomalies: of these, eight showed an improvement, of which two resulted in pregnancy; 2) Those with oligo-asthenospermia: 110 cases, with predominantly solitary varicoceles, intoxications and unknown causes: 66 per 100 showed improvement, and in 23 of these cases pregnancy resulted; 3) Those with varicoceles associated with another cause, predominantly unilateral atrophy and intoxications: 62.8 percent showed biological improvement, and 12 of these cases resulted in pregnancy. Also mentioned is the group of patients with solitary asthenospermia; solitary oligospermia and hyperzoospermia of more than 200 million per ml. Varicocele is the predominant pathology in these three groups.

Adult↗
PubMed1977

The immotile-cilia syndrome. A congenital ciliary abnormality as an etiologic factor in chronic airway infections and male sterility.

We investigated six men and a woman suspected of suffering from congenital immotility of cilia. All had chronic airway infections, and the men had immotile spermatozoa. The woman and three men had Kartagener's syndrome. The investigations included measurements of the mucociliary transport in the lower airways and ultrastructural studies of the sperm tails or respiratory cilia (or both). Mucociliary transport was significantly delayed. Sperm tails lacked dynein arms in five patients. Respiratory cilia from the women and two men lacked dynein arms and were irregularly oriented. The results support the hypothesis that a congenital defect in the cilia and sperm tails will cause chronic respiratory-tract infections and male sterility--the immotile-cilia syndrome. In about half these patients there will also be a situs inversus--i.e., Kartagener's syndrome.

Adult↗