Cytogenetic Investigation of the Rh(null) Phenotype

Vox Sanguinis ◽  
1974 ◽  
Vol 27 (2) ◽  
pp. 190-192
Author(s):  
W.L. Marsh ◽  
R.S.K. Chaganti ◽  
James German ◽  
S. Seidl ◽  
W. Spielmann
Vox Sanguinis ◽  
1974 ◽  
Vol 27 (2) ◽  
pp. 190-192
Author(s):  
W. L. Marsh ◽  
R. S. K. Chaganti ◽  
James German ◽  
S. Seidl ◽  
W. Spielmann

Mutagenesis ◽  
2006 ◽  
Vol 21 (2) ◽  
pp. 139-142 ◽  
Author(s):  
Annemarie Maes ◽  
Urbain Van Gorp ◽  
Luc Verschaeve

2000 ◽  
Vol 276 (13) ◽  
pp. 10247-10252 ◽  
Author(s):  
Lung-Chih Yu ◽  
Yuh-Ching Twu ◽  
Ching-Yi Chang ◽  
Marie Lin

1988 ◽  
Vol 23 (3) ◽  
pp. 145-148 ◽  
Author(s):  
C.P. Popescu ◽  
W.G. Smith

Transfusion ◽  
2012 ◽  
Vol 53 (3) ◽  
pp. 545-553 ◽  
Author(s):  
Zhonghui Guo ◽  
Chen Wang ◽  
Kangfeng Yan ◽  
Jingwen Xie ◽  
Wei Shen ◽  
...  

1989 ◽  
Vol 38 (2) ◽  
pp. 183
Author(s):  
Lj. Lukovic ◽  
V. Diklic ◽  
M. Kosanovic ◽  
D. Kovacevic

Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 231-243 ◽  
Author(s):  
M C Soto ◽  
T B Chou ◽  
W Bender

Abstract The genes of the Polycomb group (PcG) repress the genes of the bithorax and Antennapedia complexes, among others. To observe a null phenotype for a PcG gene, one must remove its maternal as well as zygotic contribution to the embryo. Five members of the PcG group are compared here: Enhancer of Polycomb [E(Pc)], Additional sex combs (Asx), Posterior sex combs (Psc), Suppressor of zeste 2 [Su (z) 2] and Polycomblike (Pcl). The yeast recombinase (FLP) system was used to induce mitotic recombination in the maternal germline. Mutant embryos were analyzed by staining with antibodies against six target genes of the PcG. The loss of the maternal component leads to enhanced homeotic phenotypes and to unique patterns of misexpression. E(Pc) and Su(z) 2 mutations had only subtle effects on the target genes, even when the maternal contributions were removed. Asx and Pcl mutants show derepression of the targets only in specific cell types. Psc shows unusual effects on two of the targets, Ultrabithorax and abdominal-A. These results show that the PcG genes do not act only in a common complex or pathway; they must have some independent functions.


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