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

1964 ◽  
Vol 96 (1-2) ◽  
pp. 144-144
Author(s):  
J. G. Robertson

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.

1974 ◽  
Vol 16 (4) ◽  
pp. 797-804 ◽  
Author(s):  
Earl G. Zimmerman

A chromosomal analysis of 86 specimens of Peromyscus melanophrys reveals a unique type of chromosomal difference between males and females Females possess three large pairs of subtelocentric autosomes, two pairs of small submetacentric autosomes, and 18 pairs of acrocentric autosomes. The X chromosomes are also subtelocentric. Males possess a similar karyotype with a subtelocentric X chromosome, a minute Y chromosome, and two unmatched autosomes, a large subtelocentric and a large acrocentric. Both sexes have a diploid number of 48. Studies from meiosis and autoradiography indicate that a portion of the original Y chromosome has been translocated to an autosome resulting in a new multiple sex determining mechanism in mammals, an X1X1X2X2/X1X2Y1Y2 system.


Development ◽  
1987 ◽  
Vol 101 (Supplement) ◽  
pp. 3-4
Author(s):  
Anne McLaren

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.


2020 ◽  
Vol 12 (558) ◽  
pp. eaaz5677 ◽  
Author(s):  
Emily J. Davis ◽  
Lauren Broestl ◽  
Samira Abdulai-Saiku ◽  
Kurtresha Worden ◽  
Luke W. Bonham ◽  
...  

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.


1972 ◽  
Vol 21 (1-2) ◽  
pp. 149-170
Author(s):  
Syed Shane Raza Zaidi

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.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Jingyuan Li ◽  
Rebecca McClusky ◽  
Xuqi Chen ◽  
Arthur P. Arnold ◽  
Mansoureh Eghbali

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.


1989 ◽  
Vol 37 (3) ◽  
pp. 443 ◽  
Author(s):  
G Shaw ◽  
MB Renfree ◽  
RV Short

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.


2018 ◽  
Vol 2 (1) ◽  
pp. 16-26 ◽  
Author(s):  
Nirmalchandra K. Shetty

Who is the determining factor for the sex of the offspring—mother, father, or both parents? This fundamental hypothesis proposes a new model of sex determination, challenging the existing dogma that the male Y chromosome of the father is the sole determinant of the sex of the offspring. According to modern science, the 3 X chromosomes (male XY and female XX) are assumed to be similar, and the sex of the offspring is determined after the zygote is formed. In contrast to this, the new hypothesis based on theoretical research proposes that the 3 X chromosomes can be differentiated, based on the presence of Barr bodies. The first X in female XX chromosomes and X in male XY chromosomes are similar as they lack Barr body and are hereby denoted as ‘X’ and referred to as ancestral chromosomes. The second X chromosome in the female cells which is a Barr body, denoted as X, is different. This X chromosome along with the Y chromosome are referred to as parental chromosomes. Sperm with a Y chromosome can only fuse with an ovum containing the ‘X’ chromosome. Similarly, sperm with the ‘X’ chromosome can only fuse with an ovum containing the X chromosome. Cell biology models of gametogenesis and fertilization were simulated with the new hypothesis model and assessed. Only chromosomes that participated in recombination could unite to form the zygote. This resulted in a paradigm shift in our understanding of sex determination, as both parents were found to be equally responsible for determining the sex of the offspring. The gender of the offspring is determined during the prezygotic stage itself and is dependent on natural selection. A new dimension has been given to inheritance of chromosomes. This new model also presents a new nomenclature for pedigree charts. This work of serendipity may contribute to future research in cell biology, gender studies, genome analysis, and genetic disorders including cancer.


Genetics ◽  
1989 ◽  
Vol 122 (1) ◽  
pp. 81-86 ◽  
Author(s):  
E S Walker ◽  
T W Lyttle ◽  
J C Lucchesi

Abstract In order to test whether the meiotic drive system Segregation distorter (SD) can operate on the X chromosome to exclude it from functional sperm, we have transposed the Responder locus (Rsp) to this element. This was accomplished by inducing detachments of a compound-X chromosome in females carrying a Y chromosome bearing a Rsps allele. Six Responder-sensitive-bearing X chromosomes, with kappa values ranging from 0.90 to 1.00, were established as permanent lines. Two of these have been characterized more extensively with respect to various parameters affecting meiotic drive. SD males with a Responder-sensitive X chromosome produce almost exclusively male embryos, while those with a Rsp-Y chromosome produce almost exclusively female embryos. This provides a genetic system of great potential utility for the study of early sex-specific differentiation events as it allows the collection of large numbers of embryos of a given sex.


Genetics ◽  
1979 ◽  
Vol 91 (3) ◽  
pp. 537-551
Author(s):  
L Sandler ◽  
Joseph O'Tousa

ABSTRACT Previous studies of reversed acrocentric compound-X chromosomes suggested peculiar influences of heterochromatin on both the synthesis and meiotic behavior of such compounds. It seemed, with respect to synthesis, that the long arm of the Y chromosome on an X.YL chromosome was necessary in order for the heterochromatic exchange giving rise to reversed acrocentrics to occur, even though YL itself did not participate in the compound-generating event. With respect to behavior, the resulting compounds appeared, presumably as a consequence of their singular generation, to contain an interstitial heterochromatic region that caused the distribution of exchanges between the elements of the compound to be abnormal (many zero and two-exchange tetrads with few, if any, single-exchange tetrads). Removing the interstitial heterochromatin (or, curiously, appending YL as a second arm of the compound) eliminated the recombinational anomalies and resulted in typical tetrad distributions.—We provide evidence that these peculiarities, while presumably real, were likely the consequence of a special X.YL chromosome that was used to synthesize the reversed acrocentrics examined in the early studies and are not general properties of either reversed acrocentric compounds or of interstitial heterochromatin. However, we show that specific heterochromatic regions do, in fact, profoundly influence the behavior of (apparently all) reversed acrocentric compound-X chromosomes. In particular, we demonstrate that specific portions of the Y chromosome and of the basal X-chromosome heterochromatin, when present as homologs for reversed acrocentric compounds, markedly and coordinately increase bath the frequency of exchange between the elements of the compound and the fertility (egg production) of compound-bearing females. It is, we suppose, some aspect of this heterochromatic effect, produced by the% special X.YL chromosome, that caused the earlier-analyzed compounds to exhibit the observed anomalies.


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