X-Linkage

Author(s):  
Suzanne M. Leal
Keyword(s):  
Nature ◽  
1972 ◽  
Vol 240 (5375) ◽  
pp. 14-14
Keyword(s):  

1994 ◽  
Vol 65 (4) ◽  
pp. 250-255 ◽  
Author(s):  
T.B. Nesterova ◽  
N.A. Mazurok ◽  
N.M. Matveeva ◽  
A.G. Shilov ◽  
E.I. Yantsen ◽  
...  
Keyword(s):  

Nature ◽  
1985 ◽  
Vol 316 (6029) ◽  
pp. 657-657
Author(s):  
E. Keitges ◽  
M. Rivest ◽  
M. Siniscalco ◽  
S. M. Gartler
Keyword(s):  

1969 ◽  
Vol 31 (2) ◽  
pp. 187-190 ◽  
Author(s):  
Stanley M. Garn ◽  
Keith P. Hertzog ◽  
Christabel G. Rohmann
Keyword(s):  

Genetics ◽  
1981 ◽  
Vol 97 (2) ◽  
pp. 307-325
Author(s):  
Robert H Waterston

ABSTRACT More than 30 independent suppressor mutations have been obtained in the nematode C. elegans through reversion analysis of two unc-13 mutants. Many of the new isolates map to the region of the previously identified informational suppressor, sup-5 III (Waterston and Brenner 1978). Several of the other suppressor mutations map to the left half of the X-linkage group and define a second suppressor gene, sup-7 X. In tests against 40 mutations in six genes, the sup-7(st5) allele was found to suppress to a greater extent the same alleles acted on by sup-5(e1464). Like sup-5(e1464), sup-7(st5) acts on null alleles of the myosin heavy-chain gene unc-54 I (MacLeod et al. 1977; MacLeod, Waterston and Brenner 1977) and the putative paramyosin gene unc-15 I (Waterston et al. 1977). Chemical analysis of unc-15(e1214); sup-7(st5) animals show that paramyosin is restored to more than 30% of the wild-type level. —As was observed for sup-5(e1464), suppression by sup-7(st5) is dose dependent and is greater in animals grown at 15° than at 25°. However, associated with this increased suppression is a decreased viability of sup-7(st5) homozygotes. Reversion of the lethality has resulted in the isolation of deficiency mutations that complement st5 lethality, but lack suppressor function. These properties of sup-7(st5) suggest that it, like sup-5(e1464), is an informational suppressor of null alleles, and its reversion via deficiencies further narrows the possible explanations of its action.


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