Formation of the sex chromatin by a single X-chromosome in liver cells of Rattus norvegicus

Ohno, Susumu; Kaplan, William D.; Kinosita, R.

doi:10.1016/0014-4827(59)90031-x

Cited by 325 publications

(108 citation statements)

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“…Certain properties of this inactivated chromosome, such as its late replication during the S-phase of mitosis (Taylor, 1960;Grumbach & Morishima, 1962;Mukherjee & Sinha, 1963), heteropyknosis during prophase and the formation of a sex chromatin body during interphase (Ohno, Kaplan & Kinosita, 1959;Ohno & Hauschka, 1960) have been used as criteria for establishing when the process ofinactivation begins. These features first appear in blastocysts at about the time of implantation in the cat (Austin & Amoroso, 1957), dog (Austin, 1966), rat (Zybina, 1960), hamster (Hill & Yunis, 1967), vole (Microtus agrestis) (Lee & Yunis, 1971), rhesus monkey (Macaca mulatta) (Park, 1957) and man (Glenister, 1956;Park, 1957).…”

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confidence: 99%

Sex Chromatin Formation in the Blastocyst of the Roe Deer (Capreolus Capreolus) During Delayed Implantation

Aitken¹

1974

Reproduction

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confidence: 99%

Sex Chromatin Formation in the Blastocyst of the Roe Deer (Capreolus Capreolus) During Delayed Implantation

Aitken¹

1974

Reproduction

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“…Meanwhile, it should be noted that normal females do not have G6PD activity twice as high as those of the normal males in spite of the existence of two X-chromosomes in females as compared to one in males. Based on the finding by Ohno et al (1959) that the sex chromatin in rat liver cells is comprised of a single heterochromatic X-chromosome, Beutler reasoned that if only one X-chromosome was active in each cell of a heterozygous G6PD deficiency, two types of red cells, namely, those with normal G6PD activity and those with markedly decreased activity should be produced. Beutler and Baluda (1964) treated with sodium nitrite the red cells obtained from a patient with sickle cell anemia associated with proven heterozygosity for G6PD deficiency showing about half-normal enzyme activity, then incubated the ceils with glucose and nile blue, followed by filtration by millipore filter under low oxygen pressure.…”

Section: G6pd As Genetic Markermentioning

confidence: 99%

Red cell enzyme anomalies

Shiro

1982

Jap J Human Genet

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SummaryRecent advances in the field of red cell enzyme anomalies are reviewed with a stress on G6PD as a genetic marker and on hereditary hemolytic anemia due to red cell enzyme anomalies. Using G6PD as a genetic marker, most benign and malignant tumors have been shown to have a clonal origin, except for neurofibroma and veneral warts which are clearly polyclonal. Recently, the primary structure of human red cell phosphoglycerate kinase was clarified and moreover, single amino acid substitutions of four mutant phosphoglycerate kinases were determined. To accomplish this, a method which requires only 20 ml of blood has been developed. It is a consensus among investigators in this field that the pathogenesis in three-quarters of the congenital nonspherocytic hemolytic anemia patients remain unknown even after adequate red cell enzyme studies which are now available, as well as Carrell's isopropanol test for the detection of unstable hemoglobins. IntroductionProgress in understanding red cell enzyme anomalies has been rapid in the last two decades owing to the fact that red cells are easy to obtain repeatedly from the patients and that enzymology has advanced a great deal. Since the discovery of glucose 6-phosphate dehydrogenase (G6PD) deficiency in 1956 and pyruvate kinase deficiency in 1961, 16 kinds of red cell enzyme anomalies associated with hereditary hemolytic anemia have been found so far. Moreover, it has become apparent that most, if not all, of the above-mentioned hemolytic anemias were caused by a functionally abnormal enzymes due to structural gene mutation. Single amino acid substitution was proven in a couple of G6PD variants and quite recently, in four mutant phosphoglycerate kinases. Complete amino acid sequence has been obtained in this particular enzyme recently. In this symposium, first I would like to make a brief review of the studies of G6PD as a genetic marker, followed by some recent topics of red cell enzyme anomalies mainly associated with hereditary hemolytic anemia.

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“…Fifty years ago, and building upon earlier observations by Susumo Ohno and colleagues (Ohno et al 1959), Mary Lyon proposed the random inactivation of one female X chromosome early in embryogenesis to account for the mottled phenotype of female mice heterozygous for speciWc coat colour gene mutations.…”

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confidence: 99%

Lionizing lyonization 50 years on

Cooper

2011

Hum Genet

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Formation of the sex chromatin by a single X-chromosome in liver cells of Rattus norvegicus

Cited by 325 publications

References 9 publications

Sex Chromatin Formation in the Blastocyst of the Roe Deer (Capreolus Capreolus) During Delayed Implantation

Sex Chromatin Formation in the Blastocyst of the Roe Deer (Capreolus Capreolus) During Delayed Implantation

Red cell enzyme anomalies

Lionizing lyonization 50 years on

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