Primary Genetic-Control of Sexual-Differentiation in Marsupials

1989 ◽  
Vol 37 (3) ◽  
pp. 443 ◽  
Author(s):  
G Shaw ◽  
MB Renfree ◽  
RV Short
Keyword(s):  
Genetic Control ◽  
Y Chromosome ◽  
X Chromosome ◽  
Sexual Differentiation ◽  
Hormonal Control ◽  
Sexually Dimorphic ◽  
Processus Vaginalis ◽  
X Chromosomes

Marsupials, like eutherians, normally require the presence of a Y chromosome for testicular formation. However some sexually dimorphic characters such as the scrotum, mammary anlagen, gubernaculum and processus vaginalis appear to be under direct genetic rather than secondary hormonal control. Scrota1 development occurs where only a single X chromosome is functional, whilst two X chromosomes are necessary for pouch formation.

Clues from other animals and theoretical considerations

Development ◽  
1987 ◽  
Vol 101 (Supplement) ◽  
pp. 3-4
Author(s):  
Anne McLaren
Keyword(s):  
Sex Determination ◽  
Genetic Control ◽  
Y Chromosome ◽  
X Chromosome ◽  
X Chromosomes ◽  
The Third ◽  
Mouse Species ◽  
Primary Male ◽  
Theoretical Considerations ◽  
State Of Activity

In the first two papers of this volume, the genetic control of sex determination in Caenorhabditis and Drosophila is reviewed by Hodgkin and by Nöthiger & Steinmarin-Zwicky, respectively. Sex determination in both cases depends on the ratio of X chromosomes to autosomes, which acts as a signal to a cascade of règulatory genes located either on autosomes or on the X chromosome. The state of activity of the last gene in the sequence determines phenotypic sex. In the third paper, Erickson & Tres describe the structure of the mouse Y chromosome and the polymorphisms that have been detected in different mouse species and strains. As in all mammals, the Y carries the primary male-determining locus; autosomal genes may also be involved in sex determination, but they must act down-stream from the Y-linked locus.

scholarly journals A second X chromosome contributes to resilience in a mouse model of Alzheimer’s disease

2020 ◽  
Vol 12 (558) ◽  
pp. eaaz5677 ◽  
Author(s):  
Emily J. Davis ◽  
Lauren Broestl ◽  
Samira Abdulai-Saiku ◽  
Kurtresha Worden ◽  
Luke W. Bonham ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Y Chromosome ◽  
X Chromosome ◽  
Sex Chromosome ◽  
Testicular Development ◽  
X Chromosomes ◽  
Model Of Alzheimer’S Disease ◽  
Preclinical Ad ◽  
Brain Expression

A major sex difference in Alzheimer’s disease (AD) is that men with the disease die earlier than do women. In aging and preclinical AD, men also show more cognitive deficits. Here, we show that the X chromosome affects AD-related vulnerability in mice expressing the human amyloid precursor protein (hAPP), a model of AD. XY-hAPP mice genetically modified to develop testicles or ovaries showed worse mortality and deficits than did XX-hAPP mice with either gonad, indicating a sex chromosome effect. To dissect whether the absence of a second X chromosome or the presence of a Y chromosome conferred a disadvantage on male mice, we varied sex chromosome dosage. With or without a Y chromosome, hAPP mice with one X chromosome showed worse mortality and deficits than did those with two X chromosomes. Thus, adding a second X chromosome conferred resilience to XY males and XO females. In addition, the Y chromosome, its sex-determining region Y gene (Sry), or testicular development modified mortality in hAPP mice with one X chromosome such that XY males with testicles survived longer than did XY or XO females with ovaries. Furthermore, a second X chromosome conferred resilience potentially through the candidate gene Kdm6a, which does not undergo X-linked inactivation. In humans, genetic variation in KDM6A was linked to higher brain expression and associated with less cognitive decline in aging and preclinical AD, suggesting its relevance to human brain health. Our study suggests a potential role for sex chromosomes in modulating disease vulnerability related to AD.

scholarly journals Identification of sex chromosomes using genomic and cytogenetic methods in a range-expanding spider, Argiope bruennichi (Araneae: Araneidae)

2021 ◽  
Author(s):  
Monica M Sheffer ◽  
Mathilde M Cordellier ◽  
Martin Forman ◽  
Malte Grewoldt ◽  
Katharina Hoffmann ◽  
...  
Keyword(s):  
X Chromosome ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Gc Content ◽  
Sexually Dimorphic ◽  
Behavioral Experiments ◽  
X Chromosomes ◽  
Male Karyotype ◽  
And Behavior

Differences between sexes in growth, ecology and behavior strongly shape species biology. In some animal groups, such as spiders, it is difficult or impossible to identify the sex of juveniles. This information would be useful for field surveys, behavioral experiments, and ecological studies on e.g. sex ratios and dispersal. In species with sex chromosomes, sex can be determined based on the specific sex chromosome complement. Additionally, information on the sequence of sex chromosomes provides the basis for studying sex chromosome evolution. We combined cytogenetic and genomic data to identify the sex chromosomes in the sexually dimorphic spider Argiope bruennichi, and designed RT-qPCR sex markers. We found that genome size and GC content of this spider falls into the range reported for the majority of araneids. The male karyotype is formed by 24 acrocentric chromosomes with an X1X20 sex chromosome system, with little similarity between X chromosomes, suggesting origin of these chromosomes by X chromosome fission or early duplication of an X chromosome and subsequent independent differentiation of the copies. Our data suggest similarly sized X chromosomes in A. bruennichi. They are smaller chromosomes of the complement. Our findings open the door to new directions in spider evolutionary and ecological research.

scholarly journals Neural Growth Hormone Implicated in Body Weight Sex Differences

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3826-3835 ◽  
Author(s):  
Paul J. Bonthuis ◽  
Emilie F. Rissman
Keyword(s):  
Body Weight ◽  
Sex Differences ◽  
Food Intake ◽  
X Chromosome ◽  
Sex Chromosome ◽  
Gonadal Hormones ◽  
Sexually Dimorphic ◽  
X Chromosomes ◽  
Body Weights ◽  
Neural Growth

As for many human diseases, the incidence of obesity and its associated health risks are sexually dimorphic: worldwide the rate of obesity is higher in women. Sex differences in metabolism, appetite, body composition, and fat deposition are contributing biological factors. Gonadal hormones regulate the development of many sexually dimorphic traits in humans and animals, and, in addition, studies in mice indicate a role for direct genetic effects of sex chromosome dosage on body weight, deposition of fat, and circadian timing of feeding behavior. Specifically, mice of either sex with 2 X chromosomes, typical of normal females, have heavier body weights, gain more weight, and eat more food during the light portion of the day than mice of either sex with a single X chromosome. Here we test the effects of X chromosome dosage on body weight and report that gonadal females with 2 X chromosomes express higher levels of GH gene (Gh) mRNA in the preoptic area (POA) of the hypothalamus than females with 1 X chromosome and males. Furthermore, Gh expression in the POA of the hypothalamus of mice with 2 X chromosomes correlated with body weight; GH is known to have orexigenic properties. Acute infusion of GH into the POA increased immediate food intake in normal (XY) males. We propose that X inactivation–escaping genes modulate Gh expression and food intake, and this is part of the mechanism by which individuals with 2 X chromosomes are heavier than individuals with a single X chromosome.

Psychosis, Neurosis and Epilepsy

1974 ◽  
Vol 124 (579) ◽  
pp. 144-150 ◽  
Author(s):  
P. Flor-Henry
Keyword(s):  
Y Chromosome ◽  
X Chromosome ◽  
Sexual Differentiation ◽  
Ovarian Function ◽  
Social Hierarchy ◽  
Mammalian Evolution ◽  
The Social ◽  
Critical Phase ◽  
Foetal Life ◽  
Critical Phases

It is generally accepted that in mammalian evolution from rodents to primates, including man, aggressiveness, and more particularly intra-species aggression related to the assertion of dominance in the social hierarchy of the group, is a characteristic of the male (Gray, 1971). There is also an increasing body of evidence which shows that mammalian behaviour patterns are basically female and that male patterns are determined by the action of the sex hormone testosterone on neural structures during critical phases of intra-uterine development (Seymour Levine, 1966). Ounsted and Taylor (1972) have proposed that the X chromosome is sexually neutral, essentially equivalent to an autosome, and that its role in sexual differentiation lies in that it maintains ovarian function in the female. The Y chromosome is sex-determining by causing potential autosomal and X-coded information to become manifest in the phenotype. This is achieved in part by determining the development of foetal testosterone during a critical phase of foetal life. In the absence of testosterone the fundamental female morphology would be established in either sex.

The Chromosomal Cytology of Bisexual and Parthenogenetic Calligrapha spp. (Coleoptera: Chrysomelidae)

1964 ◽  
Vol 96 (1-2) ◽  
pp. 144-144
Author(s):  
J. G. Robertson
Keyword(s):  
Y Chromosome ◽  
X Chromosome ◽  
Diploid Number ◽  
Testicular Tissue ◽  
Reduction Division ◽  
Bisexual Species ◽  
X Chromosomes ◽  
Metaphase I

Thirty-one geographic entities comprising 17 species of Calligrapha were examined cytologically. In the bisexual species rowena, philadelphica, pnirsa, amator, alni, confluens, californica, bidenticola, multipunctata, verrucosa, and pruni, the diploid number of chromosomes was 23 in males and 24 in females. The sex mechanism consisted of a single X chromosome in males and two X chromosomes in females. No Y chromosome was present. During reduction division in testicular tissue 11 bivalents were formed and a single heterochromatic X chromosome lay to one side of the bivalents which showed congression at metaphase I. The basic chromosomal formula 11 + XO can therefore be assigned to this group. The formula is modified in some populations according to the following circumstances.

Genetic control of sex-chromosomal univalency in the spermatocytes of C57BL/6J and DBA/2J mice

1985 ◽  
Vol 27 (6) ◽  
pp. 741-750 ◽  
Author(s):  
F. G. Biddle ◽  
B. G. MacDonald ◽  
B. A. Eales
Keyword(s):  
Genetic Control ◽  
Y Chromosome ◽  
X Chromosome ◽  
Genetic Factors ◽  
Additive Effect ◽  
Unknown Number ◽  
Attachment Sites ◽  
Sufficient Distance ◽  
Strain Pair ◽  
Reciprocal Backcross

The genetic control of sex-chromosomal univalency was examined in the primary spermatocytes of the mouse. The C57BL/6J strain expresses 3% X–Y univalency and DBA/2J expresses 37% univalency. The reciprocal F1 and the eight types of reciprocal backcross males were examined. In the C57BL/6J–DBA/2J strain pair, X–Y univalency is controlled by three genetic systems. Autosomal factors of unknown number that are dominant in DBA/2J increase the probability of univalency from 3% in C57BL/6J to 12%. The DBA/2J-Y chromosome, in place of the C57BL/6J-Y chromosome, has an additive effect to increase the probability of univalency from 12 to 37% in the DBA/2J strain. Two X-chromosome factors that differ between C57BL/6J and DBA/2J regulate the probability of univalency. The X-chromosome factors appear to be separated by sufficient distance so that, with the DBA/2J-Y chromosome and dominant DBA/2J autosomal factors, there are two recombinant classes of X–Y univalency at 20 and 60%. The genetic factors in the univalency trait may be involved in the regulation or structure of the terminal attachment sites between the X and Y chromosomes.Key words: meiosis, mouse, sex-chromosomal univalency.

Determination of Sex Chromatin — A New Concept

1972 ◽  
Vol 21 (1-2) ◽  
pp. 149-170
Author(s):  
Syed Shane Raza Zaidi
Keyword(s):  
Sex Determination ◽  
Y Chromosome ◽  
X Chromosome ◽  
Mother Cell ◽  
Daughter Cell ◽  
Barr Body ◽  
X Chromosomes ◽  
Sex Chromatin

SummaryInstead of the random activation and/or inactivation of the X-chromosome in sex determination, as suggested by the Lyon's hypothesis, a proposal is made here that crossingover between the sister- and/or nonsisterstrands at the sticky or nonsticky loci, at heterochromatinizing regions and at the inactivating centers of the centromère, be responsible for the heterochromatinization and/or heteropyknotization of the X-chromosome. (This proposal will be called the Mustafa hypothesis.)Such would be the basis for the activation and/or inactivation of the X-chromatid(s), which would then replicate into a normal or a heterochromatic X-chromosome respectively. The heterochromatic X-chromosome may be transformed into a heteropyknotized mass of sex chromatin (Barr body). Translocation of the Y-chromosome and of some of the autosomes could also result in the same effect. Hence, the number of heterochromatinized X-chromosomes, and/or of heteropyknotized masses (Barr bodies), in each daughter-cell is directly proportional to half the number of chromatids involved in crossingover and/or translocation in the mother-cell.

Genetics of sex determination: what can we learn from Drosophila?

Development ◽  
1987 ◽  
Vol 101 (Supplement) ◽  
pp. 17-24
Author(s):  
Rolf Nöthiger ◽  
Monica Steinmann-Zwicky
Keyword(s):  
Molecular Biology ◽  
Sex Determination ◽  
Genetic Control ◽  
Sexual Development ◽  
Sexual Differentiation ◽  
Regulatory Elements ◽  
Negative Control ◽  
Homeotic Genes ◽  
Specific Expression ◽  
X Chromosomes

The combined efforts of genetics, developmental and molecular biology have revealed the principles of genetic control of sexual differentiation in Drosophila. In combination with maternal components, a quantitative chromosomal signal, provided by the ratio of X chromosomes to sets of autosomes (X: A), regulates a key gene (Sxl). The functional state, ON or OFF, of Sxl, via a few subordinate regulatory genes, controls a switch gene (dsx) that can express two mutually exclusive functions, M or F. These serve to repress either the female or the male set of differentiation genes, thus directing the cells either into the male or into the female sexual pathway. Investigations of control genes and their regulation show that they have properties of homeotic genes. Their role is to select one of two alternative developmental programs. Their function, or lack of function, is required throughout development to maintain the cells in their respective sexual pathway. Differentiation genes are under negative control by dsx. We discuss the cis- and tams-regulatory elements that are needed for sex-, tissue- and stage-specific expression of the differentiation genes. A comparison of Drosophila to other organisms such as Caenorhabditis, mammals and other insects indicates similarities that we interpret as evidence for a basically invariant genetic strategy used by various organisms to regulate sexual development.

Abstract 216: Sex Chromosome Protection Again Myocardial Ischemia/reperfusiong Injury In Mice: One X Is Better Than Two

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Jingyuan Li ◽  
Rebecca McClusky ◽  
Xuqi Chen ◽  
Arthur P. Arnold ◽  
Mansoureh Eghbali
Keyword(s):  
Sex Differences ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Y Chromosome ◽  
X Chromosome ◽  
Functional Recovery ◽  
Ischemia Reperfusion ◽  
Gonadal Hormones ◽  
Xy Model ◽  
X Chromosomes

Sex differences in susceptibility to ischemia/reperfusion (I/R) injury have been demonstrated both in basic and clinical settings. Female hearts show better functional recovery after I/R injury compared with males. Most of these sex differences in the I/R injury model have been attributed to sex hormones. Here we used a unique mouse model (XY*) to investigate the role of sex chromosomes on cardiac I/R injury. The XY* model produces the equivalent of XX and XO gonadal females, and XY and XXY gonadal males. A comparison between mice with one X chromosome (XO or XY) to those with two X chromosomes (XX or XXY) reveals an effect of X chromosome number, whereas comparing mice with a Y chromosome (XY, XXY) with those without Y (XO, XX) shows the effect of presence/absence of the Y chromosome. Four to six weeks before the experiment, mice were gonadectomized (GDX) to eliminate the effects of gonadal hormones. Isolated mouse hearts were subjected to 30 min global normothermic ischemia followed by 60 min reperfusion. Hemodynamic parameters were continuously recorded with a catheter (1.4F Millar SPR-671) connected to a pressure transducer (Power Lab, ADInstruments). At the end of reperfusion, the hearts were cut into four transverse slices and myocardial necrosis was assessed by measurement of the infarct size using triphenyltetrazolium chloride (TTC) staining. The cardiac function was similar among all 4 groups of XY* mice before ischemia. However, postischemic functional recovery of mice with two copies of the X chromosome was significantly lower than mice with a single copy, irrespective of gonadal sex. Rate pressure product (RPP) recovery was markedly lower in XX gonadal females (34.0±10.3%, n=6) and XXY gonadal males (28.0±12.1%, n=5) compared to XO females (60.3±13.5%, n=4) and XO males (60.5±13.8%, n=5, p<0.05). Infarct size was also markedly larger in mice with two X chromosomes (41.4±8.9% in XX gonadal females (n=6) and 46.3±9.5% in XXY gonadal males (n=5)) than mice with one X chromosome (23.7±3.9% in XO females, n=4 and 26.6±6.9% in XO males, n=5, p<0.05). In conclusion, the number of X chromosomes in gonadectomized mice plays a key role in susceptibility to myocardial ischemia/reperfusion injury regardless of the presence or absence of the Y chromosome.

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