Demonstration of 2n spermatids in carriers of the ?sex reversed? factor in the mouse by feulgen cytophotometry

1980 ◽  
Vol 69 (3) ◽  
pp. 299-306 ◽  
Author(s):  
E. Hannappel ◽  
W. Siegler ◽  
U. Drews

1972 ◽  
Vol 5 (3) ◽  
pp. 146-152 ◽  
Author(s):  
SETSUYA FUJITA ◽  
MASARU FUKUDA ◽  
TADAHISA KITAMURA ◽  
SATORU YOSHIDA


1968 ◽  
Vol 43 (2) ◽  
pp. 111-117 ◽  
Author(s):  
M. S. Greenwood ◽  
G. P. Berlyn


1971 ◽  
Vol 50 (3) ◽  
pp. 669-681 ◽  
Author(s):  
G. Le M. Campbell ◽  
H. Weintraub ◽  
B. H. Mayall ◽  
H. Holtzer

Primitive erythroblasts in the circulating blood of the chick embryo continue to divide while synthesizing hemoglobin (Hb). Hb measurements on successive generations of erythroblasts show that there is a progressive increase in the Hb content of both interphase and metaphase cells. Furthermore, for any given embryo the Hb content of metaphase cells is always significantly greater than that of interphase cells. The distribution of Hb values for metaphase cells suggests that there are six Hb classes corresponding to the number of cell cycles in the proliferative phase. The location of erythroblasts in the cell cycle was determined by combining Feulgen cytophotometry with thymidine radioautography on the same cells. Measurements of the Hb content for erythroblasts in different compartments of the cell cycle (G1, S, G2, and M) show a progressive increase through the cycle. Thus, the amount of Hb per cell is a function of the number of cell divisions since the initiation of Hb synthesis and, to a lesser degree, the stage of the cell cycle. Earlier generations of erythroblasts synthesize Hb at a faster rate than the terminal generation. Several models have been proposed to explain these findings.



Genome ◽  
1989 ◽  
Vol 32 (3) ◽  
pp. 389-392 ◽  
Author(s):  
Sarmistha Sen ◽  
Geeta Talukder ◽  
Archana Sharma

Chromosome analysis of bone marrow cells from 96 sex-matched Rattus norvegicus of 12 different age groups showed a significant increase in hypodiploid cells with ageing. However, in meiotic preparations from gonadal cells of male rats the frequency of hypodiploid or hyperdiploid cells did not change significantly. In situ DNA estimation of bone marrow nuclei, following Feulgen cytophotometry, also did not show any significant difference with gradual age changes.Key words: senescence, DNA content, age-related changes.



1979 ◽  
Vol 54 (4) ◽  
pp. 201-204 ◽  
Author(s):  
Graeme P. Berlyn ◽  
Sukhraj S. Dhillon ◽  
Jerome P. Miksche




1986 ◽  
Vol 48 (2) ◽  
pp. 65-75 ◽  
Author(s):  
A. S. Mukherjee ◽  
Mita Ghosh

SummaryThe transcriptional competence of the X-chromosome of a mutant strain of Drosophila melanogaster, [in(1)BM2 (reinverted)], and of hyperploid derivatives with different additional segments of the X-chromosome has been examined. The single X in the mutant male shows twice as much puffiness and RNA synthesis as does that in the normal male, revealing a level of X-coded activity in addition to the normal male and female levels. Feulgen cytophotometry reveals no duplication of DNA content in the mutant X. When duplication for the segments 1A-3E, 9A-20F, 11A-20F and 16A-20F of the X-chromosome are combined in the male with the mutant chromosome, the super-hyperactivity of the mutant X is completely abolished. In combination with the Bs. Y duplication, which contains 16A7-B2, the two-fold activity is also completely suppressed.The mutant chromosome can appear in three discrete manifestations, namely, highly flabby, intermittently flabby and normal, suggesting a leaky nature of the mutant. The effect is also temperature-sensitive. Our results suggest that there may be a modulator gene complex (M+) in the 16A7-B2 region as well as regulators elsewhere on the X, which in combination influence the hyperactivity of the male X in Drosophila. We suggest that the In(1)BM2 (reinverted) chromosome carries a hypomorphic mutation of M+(Mm). The results presented here and earlier data on various X-chromosomal and autosomal hyperploids are discussed in the light of a model for dosage compensation in Drosophila.



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