Y chromosome replication and chromosome arrangement in germ line cells and sperm of the rat

Chromosoma ◽  
1969 ◽  
Vol 28 (3) ◽  
pp. 370-378 ◽  
Author(s):  
N. O. Bianchi ◽  
Martha S. de Bianchi
Keyword(s):  
Y Chromosome ◽  
Germ Line ◽  
Chromosome Replication ◽  
Chromosome Arrangement

scholarly journals Drosophila melanogaster male germ line-specific transcripts with autosomal and Y-linked genes.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 293-308 ◽  
Author(s):  
S R Russell ◽  
K Kaiser
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Germ Line ◽  
Stop Codon ◽  
Chromatin Condensation ◽  
Sperm Chromatin ◽  
Autosomal Gene ◽  
Cdna Clones ◽  
Autosomal Locus ◽  
Functional Protein

Abstract We have identified of set of related transcripts expressed in the germ line of male Drosophila melanogaster. Surprisingly, while one of the corresponding genes is autosomal the remainder are located on the Y chromosome. The autosomal locus, at 77F on chromosome arm 3L, corresponds to the previously described transcription unit 18c, located in the first intron of the gene for an RI subunit of cAMP-dependent protein kinase. The Y chromosome copies have been mapped to region h18-h19 on the cytogenetic map of the Y outside of any of the regions required for male fertility. In contrast to D. melanogaster, where Y-linked copies were found in nine different wild-type strains, no Y-linked copies were found in sibling species. Several apparently Y-derived cDNA clones and one Y-linked genomic clone have been sequenced. The Y-derived genomic DNA shares the same intron/exon structure as the autosomal copy as well as related flanking sequences suggesting that it transposed to the Y from the autosomal locus. However, this particular Y-linked copy cannot encode a functional polypeptide due to a stop codon at amino acid position 72. Divergence among five different cDNA clones ranges from 1.5 to 6% and includes a large number of third position substitutions. We have not yet obtained a full-length cDNA from a Y-linked gene and therefore cannot conclude that the D. melanogaster Y chromosome contains functional protein-coding genes. The autosomal gene encodes a predicted polypeptide with 45% similarity to histones of the H5 class and more limited similarity to cysteine-rich protamines. This protein may be a distant relative of the histone H1 family perhaps involved in sperm chromatin condensation.

Timing of Sex Chromosome Replication in Somatic and Germ-Line Cells of the Mouse and the Rat

1967 ◽  
Vol 6 (1) ◽  
pp. 51-66 ◽  
Author(s):  
L. Tiepolo ◽  
M. Fraccaro ◽  
Maj Hultén ◽  
J. Lindsten ◽  
Anna Mannini ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Germ Line ◽  
Chromosome Replication

scholarly journals Oxidative stress, DNA damage and the Y chromosome

Reproduction ◽  
2001 ◽  
pp. 497-506 ◽  
Author(s):  
RJ Aitken ◽  
C Krausz
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Y Chromosome ◽  
Nuclear Dna ◽  
Germ Line ◽  
Reactive Oxygen Species Generation ◽  
High Rate ◽  
Severe Oligozoospermia ◽  
Gene Deletions ◽  
Chromosome Deletions

Recent advances in understanding of male infertility have implicated two major causative factors, oxidative stress and Y chromosome deletions. A major cause of oxidative stress appears to be the high rate of reactive oxygen species generation associated with the retention of excess residual cytoplasm in the sperm midpiece. Other possible causes include the redox cycling of xenobiotics, and antioxidant depletion or apoptosis. Oxidative stress induces peroxidative damage in the sperm plasma membrane and DNA damage in both the mitochondrial and nuclear genomes. Nuclear DNA damage in the germ line of the father may be associated with pathology in the offspring, including childhood cancer and infertility. Gene deletions on the non-recombining region of the Y chromosome account for the infertility observed in about 15% of patients with azoospermia and 5-10% of subjects with severe oligozoospermia. The Y chromosome is particularly susceptible to gene deletions because of the inability of the haploid genome to deploy recombination repair in retrieving lost genetic information. Aberrant recombination, defective chromatin packaging, abortive apoptosis and oxidative stress may all be involved in the aetiology of DNA damage in the germ line. The factors responsible for Y chromosome deletions in spermatozoa remain unresolved but may be one facet of a central reproductive problem: controlling the amount of oxidative stress experienced by germ cells during their differentiation and maturation in the male reproductive tract.

scholarly journals AZFa candidate gene UTY and its X homologue UTX are expressed in human germ cells

2021 ◽  
Author(s):  
Peter H Vogt ◽  
Jutta Zimmer ◽  
Ulrike Bender ◽  
Thomas Strowitzki
Keyword(s):  
Germ Cell ◽  
Candidate Gene ◽  
Y Chromosome ◽  
Germ Cells ◽  
Protein Interactions ◽  
Germ Line ◽  
Primordial Germ Cells ◽  
Basal Membrane ◽  
Specific Protein ◽  
Disorders Of Sexual Development

The Ubiquitous Transcribed Y (UTY) AZFa candidate gene on the human Y chromosome and its paralog on the X chromosome, UTX, encode a histone lysine demethylase removing chromatin H3K27 methylation marks at genes transcriptional start sites for activation. Both proteins harbour the conserved Jumonji C (JmjC) domain, functional in chromatin metabolism, and an extended N-terminal tetratrico peptide repeat (TPR) block involved in specific protein-interactions. Specific antisera for human UTY and UTX proteins were developed to distinguish expression of both proteins in human germ cells by immunohistochemical experiments on appropriate tissue sections. In the male germ line, UTY was expressed in the fraction of A spermatogonia located at the basal membrane probably including spermatogonia stem cells. UTX expression was more spread in all spermatogonia and in early spermatids. In female germ line, UTX expression was found in the primordial germ cells of the ovary. UTY was also expressed during fetal male germ cell development, whereas UTX expression was visible only at distinct gestation weeks. Based on these results and the conserved neighboured location of UTY and DDX3Y in Yq11 found in mammals of distinct lineages, we conclude that UTY –like DDX3Y- is part of the Azoospermia factor a (AZFa) locus functioning in human spermatogonia to support the balance of their proliferation-differentiation rate before meiosis. Comparable UTY and DDX3Y expression was also found in gonadoblastoma and dysgerminoma cells found in germ cell nests of the dysgenetic gonads of individuals with disorders of sexual development and a Y chromosome in karyotype (DSD-XY). This confirms that AZFa overlaps with GBY, the Gonadoblastoma susceptibility Y locus, and includes the UTY gene.

scholarly journals Imprinting of the Y Chromosome Influences Dosage Compensation in roX1 roX2 Drosophila melanogaster

Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 811-820 ◽  
Author(s):  
Debashish U. Menon ◽  
Victoria H. Meller
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Dosage Compensation ◽  
Sex Chromosome ◽  
Germ Line ◽  
Chromatin Modification ◽  
Regulatory System ◽  
The Body ◽  
Autosomal Gene ◽  
Y Chromosomes

Drosophila melanogaster males have a well-characterized regulatory system that increases X-linked gene expression. This essential process restores the balance between X-linked and autosomal gene products in males. A complex composed of the male-specific lethal (MSL) proteins and RNA is recruited to the body of transcribed X-linked genes where it modifies chromatin to increase expression. The RNA components of this complex, roX1 and roX2 (RNA on the X1, RNA on the X2), are functionally redundant. Males mutated for both roX genes have dramatically reduced survival. We show that reversal of sex chromosome inheritance suppresses lethality in roX1 roX2 males. Genetic tests indicate that the effect on male survival depends upon the presence and source of the Y chromosome, revealing a germ line imprint that influences dosage compensation. Conventional paternal transmission of the Y chromosome enhances roX1 roX2 lethality, while maternal transmission of the Y chromosome suppresses lethality. roX1 roX2 males with both maternal and paternal Y chromosomes have very low survival, indicating dominance of the paternal imprint. In an otherwise wild-type male, the Y chromosome does not appreciably affect dosage compensation. The influence of the Y chromosome, clearly apparent in roX1 roX2 mutants, thus requires a sensitized genetic background. We believe that the Y chromosome is likely to act through modulation of a process that is defective in roX1 roX2 mutants: X chromosome recognition or chromatin modification by the MSL complex.

scholarly journals The Male-Determining Activity on the Y Chromosome of the Housefly (Musca domestica L.) Consists of Separable Elements

Genetics ◽  
1998 ◽  
Vol 150 (2) ◽  
pp. 651-661
Author(s):  
Monika Hediger ◽  
Ariane Denise Minet ◽  
Markus Niessen ◽  
Regula Schmidt ◽  
Denise Hilfiker-Kleiner ◽  
...  
Keyword(s):  
Y Chromosome ◽  
Maternal Effect ◽  
Germ Line ◽  
C Banding ◽  
Female Germ Line ◽  
The Common ◽  
Pole Cells ◽  
Different Strains ◽  
Autosomal Translocation ◽  
Determining Factor

Abstract In the common housefly, the presence or absence of a male-determining factor, M, is responsible for sex determination. In different strains, M has been found on the Y, on the X, or on any of the five autosomes. By analyzing a Y-autosomal translocation and a ring-shaped, truncated Y chromosome, we could show that M on the Y consists of at least two regions with M activity: One of them can be assigned to the short arm of the Y chromosome (MYS), which is largely C-banding negative, the other region lies on the C-banding positive long arm of the Y, including the centromeric part (MYL). Each region alone behaves as a hypomorphic M factor, causing many carriers to develop as intersexes of the mosaic type instead of as males. When introduced into the female germ line by transplantation of progenitor germ cells (pole cells), the MYS shows an almost complete maternal effect that predetermines 96% of the genotypic female (NoM) animals to develop as males. In contrast, the MYL has largely lost its maternal effect, and most of the NoM animals develop as females. Increasing the amount of product made by either of the two hypomorphic M factors (by combining the MYS and MYL or two MYS) leads to complete male development in almost every case. We thus assume that the Y chromosome carries at least two copies of M, and that these are functionally equivalent.

scholarly journals Y-Linked Male Sterile Mutations Induced by P Element in Drosophila melanogaster

Genetics ◽  
1998 ◽  
Vol 150 (2) ◽  
pp. 735-744 ◽  
Author(s):  
Ping Zhang ◽  
Rebecca L Stankiewicz
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Insertional Mutagenesis ◽  
Germ Line ◽  
Position Effect ◽  
Repetitive Sequences ◽  
P Element ◽  
Dependent Manner ◽  
Male Sterile ◽  
Structural And Functional Properties

Abstract The Y chromosome in Drosophila melanogaster is composed of highly repetitive sequences and is essential only in the male germ line. We employed P-element insertional mutagenesis to induce male sterile mutations in the Y chromosome. By using a combination of two modifiers of position effect variegation, adding an extra Y chromosome and increasing temperature, we isolated 61 P(ry+) elements in the Y chromosome. Six of these Y-linked insertions (approximately 10%) induced male sterile mutations that are mapped to two genes on the long and one on the short arms of the Y chromosome. These mutations are revertible to the wild type in a cell-autonomous and germ-line-dependent manner, consistent with previously defined Y-linked gene functions. Phenotypes associated with these P-induced mutations are similar to those resulting from deletions of the Y chromosome regions corresponding to the male fertility genes. Three alleles of the kl-3 gene on the Y long arm result in loss of the axonemal outer dynein arms in the spermatid tail, while three ks-2 alleles on the Y short arm induce defects at early postmeiotic stages. The recovery of the ms(Y) mutations induced by single P-element insertions will facilitate our effort to understand the structural and functional properties of the Y chromosome.

The role of the mammalian Y chromosome in spermatogenesis

Development ◽  
1987 ◽  
Vol 101 (Supplement) ◽  
pp. 133-141
Author(s):  
Paul S. Burgoyne
Keyword(s):  
Y Chromosome ◽  
Germ Cells ◽  
Germ Line ◽  
Fetal Life ◽  
Chromosomal Gene ◽  
Male Germ Line ◽  
Germ Cell Differentiation ◽  
Sperm Abnormalities ◽  
Male Phenotype

All aspects of the mammalian male phenotype are due either directly or indirectly to Y-chromosome activity. This review summarizes what is known of the role of the Y in male germ cell differentiation in the mouse. The initial diversion of germ cells to the male pathway in fetal life (that is the formation of amitotic T1-prospermatogonia rather than meiotic oocytes) is an indirect effect of the Y: the Y-chromosomal testis determining gene (Tdy) acts to create a testis and the testicular environment causes the germ cells to follow the male pathway. XX and XO germ cells can therefore form T1-prospermatogonia, but the extra X of XX prospermatogonia in some way causes their death perinatally. The first direct effect of the Y in the germ line occurs at the initiation of the spermatogenic cycles (approx. 1 week after birth) when a Y-chromosomal gene (Spy) is needed for normal spermatogonial survival and progression to meiosis. Spy is present in the Y-derived Sxr fragment so XOSxr germ cells enter meiosis normally. An Sxr derivative, Sxr′, which has lost the capacity to produce H-Y antigen, has also lost the Spy function, raising the possibility that H-Y antigen is the mediator of Spy activity. The Y is next required in the male germ line during meiotic prophase, when it provides a pairing partner for the X chromosome. If the X (or, indeed, the Y when present) remains unpaired, there are severe spermatogenic losses and the second meiotic division is frequently omitted, leading to the formation of diploid spermatids. Spermatogenesis in XOSxr males is affected in this way and the few sperm produced are morphologically abnormal. These sperm abnormalities could also be a consequence of the X univalence, but there is some evidence suggesting that there is another gene on the Y, lacking in Sxr, which is involved in sperm morphogenesis.

INTRASPECIES AUTOSOMAL POLYMORPHISM AND CHROMOSOME REPLICATION IN AKODON MOLINAE (RODENTIA: CRICETIDAE)

1969 ◽  
Vol 11 (2) ◽  
pp. 233-242 ◽  
Author(s):  
N. O. Bianchi ◽  
J. Contreras ◽  
F. N. Dulout
Keyword(s):  
Bone Marrow ◽  
Y Chromosome ◽  
X Chromosome ◽  
Sex Chromosome ◽  
Chromosome Analysis ◽  
Chromosome Replication ◽  
Chromosome 1 ◽  
Submetacentric Chromosome ◽  
Sex Chromatin ◽  
S Period

Cell spreads from bone marrow, spleen, testis and liver of four male and four female Akodon molinae (Rodentia:Cricetidae) were used for chromosome analysis and sex chromatin scoring. Chromosome replication at the beginning and end of the S period were analysed in bone marrow cells.In five animals (three males and two females) the diploid chromosome number was 42; the other three (1 male and 2 females) had a modal number of 43. In the former animals pairs 1,2,19,20 and the Y chromosome were easily identified morphologically. Chromosomes 1 were large and metacentric. In specimens with 43 chromosomes, pairs 2-20-XY were similar to those of animals with 42. Instead of having two number 1 homologues, these animals showed three unpaired chromosomes, one chromosome 1, one subterminal chromosome (1a) homologue of the long arm of the chromosome 1 and one submetacentric chromosome (1b) homologue of the short arm of the chromosome 1 Chromosomes 1a and 1b were considered to have arisen by a Robertsonian mechanism of centric fission of chromosome 1 plus a pericentric inversion.Studies of sex chromosome replication showed that the Y chromosome was the last to start and to end DNA synthesis in male complements. In females one X chromosome was the last to start replication. No late replicating X chromosome at the end of the S period was found. Coincidently, no sex chromatin could be detected in females.Analysis of late replication patterns in chromosomes 1, 1a and 1b, indicates that pericentric inversions can shift the replicating moment of the chromosomal regions involved in the rearrangement.

scholarly journals Differential timing of S phases, X chromosome replication, and meiotic prophase in the C. elegans germ line

2007 ◽  
Vol 308 (1) ◽  
pp. 206-221 ◽  
Author(s):  
Aimee Jaramillo-Lambert ◽  
Marina Ellefson ◽  
Anne M. Villeneuve ◽  
JoAnne Engebrecht
Keyword(s):  
X Chromosome ◽  
Meiotic Prophase ◽  
Germ Line ◽  
Chromosome Replication ◽  
C Elegans ◽  
Differential Timing
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