zygotic induction
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2020 ◽  
Vol 11 ◽  
Author(s):  
Masatoshi Miyakoshi ◽  
Yoshiyuki Ohtsubo ◽  
Yuji Nagata ◽  
Masataka Tsuda


1992 ◽  
Vol 6 (5) ◽  
pp. 605-613 ◽  
Author(s):  
A. Louise Jones ◽  
Peter T. Barth ◽  
Brian M. Wilkins


1982 ◽  
Vol 187 (2) ◽  
pp. 231-235 ◽  
Author(s):  
Sheldon I. Feinstein ◽  
K. Brooks Low
Keyword(s):  
E Coli ◽  




1975 ◽  
Vol 25 (2) ◽  
pp. 179-187 ◽  
Author(s):  
K. E. Carey ◽  
V. Krishnapillai

SUMMARYThe UV-inducible prophage J51 has been mapped late on the chromosome ofP. aeruginosastrain PAO, relative to the entry point of the sex factor FP2. This was determined following the analysis of the segregation of unselected markers in conjugational crosses between appropriately marked donor and recipient strains. A more precise location of about 50 min was obtained from the kinetics of increase in infectious centres due to zygotic induction during interrupted mating experiments.



1974 ◽  
Vol 23 (2) ◽  
pp. 155-164 ◽  
Author(s):  
K. E. Carey ◽  
V. Krishnapillai

SUMMARYProphage H90 has been found to undergo a phenomenon similar to zygotic induction, during conjugal transfer from a lysogenic donor to a non-lysogenic recipient.It has not been possible to demonstrate that the level of infectious centres increases concomitantly with transfer of the prophage. However, the genetic consequence of zygotic induction was observed with regard to decreased recombinant yield of markers distal to the prophage. This latter fact has been exploited in interrupted mating experiments, to locate the prophage at between 5 and 7 min on thePseudomonas aeruginosastrain PAO map. It was further shown by transduction experiments that the prophage does not appear to be linked to clusters of co-transductional markers at the 5 and 7 min locations.



1973 ◽  
Vol 123 (4) ◽  
pp. 355-361
Author(s):  
Vladimír Špelina ◽  
Zdeněk Neubauer ◽  
Vojtěch Závada


1969 ◽  
Vol 13 (2) ◽  
pp. 227-240 ◽  
Author(s):  
S. W. Glover ◽  
C. Colson

The sites of mutations affecting host-controlled modification (HCM) have been mapped inE. coliK andE. coliB by conjugation and transduction experiments between mutants. These mutations all map close to theserBlocus on the opposite side to the markerthr. Non-parental HCM has been observed among colonies obtained from Pl transduction experiments between HCM mutants. Control experiments have shown that these non-parental recombinants can not be accounted for by reversion of either parent and must result from recombination between mutants. Several genetic models are suggested which could account for these recombinants and an attempt is made to distinguish between various models by testing for complementation between mutants in a zygotic induction complementation test.



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