scholarly journals Behavior of three colicine factors and an R (drug-resistance) factor in Hfr crosses inSalmonella typhimurium

1967 ◽  
Vol 9 (3) ◽  
pp. 283-297 ◽  
Author(s):  
Eugenie Dubnau ◽  
B. A. D. Stocker

An LT2 Hfr strain,his metC gal, was crossed to a multiply marked LT2 F−line. Analysis of recombinant yields, segregation of unselected markers and interrupted matings indicated injection of the Hfr chromosome in the sequenceThe introduction into the Hfr of the colicine factorscolI, colE1andcolE2and the R factorR2had little or no effect on its fertility. All four factors were transmitted at low frequency to the F−population, and to recombinants at higher frequencies (colI5–30%,colE130–80%,colE25–30%,R20–9%). Transfer ofcolE1occurred before 20 min., that ofcolE2andcolIlater than 100 min. Segregation data did not reveal close linkage of any factor to any chromosomal locus, but recombinants with a long stretch of donor chromosome were more likely than others to have acquiredcolE2andcolI. Nearly all recombinants andF−cells which acquiredcolIorcolE2acquired both, andcolE1also. Most cells which acquiredR2acquired one or more colicine factors. These plasmid associations can be formally represented by transfer of plasmids, independently of the chromosome, in the sequencecolE1—(colI, colE2)—R2. Phage P22 grown on the Hfr carrying the four plasmids transduced thetet-rtrait ofR2at very low frequency, and thesul-r str-rcharacters, together, at low frequency. Some of each sort of drug-resistance transductant, but no transductants in respect of chromosomal characters, acquiredcolEl or colE2by co-transduction.

2015 ◽  
Author(s):  
Yong Tao ◽  
Zheng Hu ◽  
Shaoping Ling ◽  
Shiou-Hwie Yeh ◽  
Weiwei Zhai ◽  
...  

The genetic diversity within a single tumor can be extremely large, possibly with mutations at all coding sites (Ling et al. 2015). In this study, we analyzed 12 cases of multiple hepatocellular carcinoma (HCC) tumors by sequencing and genotyping several samples from each case. In 10 cases, tumors are clonally related by a process of cell migration and colonization. They permit a detailed analysis of the evolutionary forces (mutation, migration, drift and natural selection) that influence the genetic diversity both within and between tumors. In 23 inter-tumor comparisons, the descendant tumor usually shows a higher growth rate than the parent tumor. In contrast, neutral diversity dominates within-tumor observations such that adaptively growing clones are rarely found. The apparent adaptive evolution between tumors can be explained by the inherent bias for detecting larger tumors that have a growth advantage. Beyond these tumors are a far larger number of clones which, growing at a neutral rate and too small to see, can nevertheless be verified by molecular means. Given that the estimated genetic diversity is often very large, therapeutic strategies need to take into account the pre-existence of many drug-resistance mutations. Importantly, these mutations are expected to be in the very low frequency range in the primary tumors (and become frequent in the relapses, as is indeed reported (1-3). In conclusion, tumors may often harbor a very large number of mutations in the very low frequency range. This duality provides both a challenge and an opportunity for designing strategies against drug resistance (4-8).


2009 ◽  
Vol 23 (4) ◽  
pp. 191-198 ◽  
Author(s):  
Suzannah K. Helps ◽  
Samantha J. Broyd ◽  
Christopher J. James ◽  
Anke Karl ◽  
Edmund J. S. Sonuga-Barke

Background: The default mode interference hypothesis ( Sonuga-Barke & Castellanos, 2007 ) predicts (1) the attenuation of very low frequency oscillations (VLFO; e.g., .05 Hz) in brain activity within the default mode network during the transition from rest to task, and (2) that failures to attenuate in this way will lead to an increased likelihood of periodic attention lapses that are synchronized to the VLFO pattern. Here, we tested these predictions using DC-EEG recordings within and outside of a previously identified network of electrode locations hypothesized to reflect DMN activity (i.e., S3 network; Helps et al., 2008 ). Method: 24 young adults (mean age 22.3 years; 8 male), sampled to include a wide range of ADHD symptoms, took part in a study of rest to task transitions. Two conditions were compared: 5 min of rest (eyes open) and a 10-min simple 2-choice RT task with a relatively high sampling rate (ISI 1 s). DC-EEG was recorded during both conditions, and the low-frequency spectrum was decomposed and measures of the power within specific bands extracted. Results: Shift from rest to task led to an attenuation of VLFO activity within the S3 network which was inversely associated with ADHD symptoms. RT during task also showed a VLFO signature. During task there was a small but significant degree of synchronization between EEG and RT in the VLFO band. Attenuators showed a lower degree of synchrony than nonattenuators. Discussion: The results provide some initial EEG-based support for the default mode interference hypothesis and suggest that failure to attenuate VLFO in the S3 network is associated with higher synchrony between low-frequency brain activity and RT fluctuations during a simple RT task. Although significant, the effects were small and future research should employ tasks with a higher sampling rate to increase the possibility of extracting robust and stable signals.


1988 ◽  
Author(s):  
Wayne I. Klemetti ◽  
Paul A. Kossey ◽  
John E. Rasmussen ◽  
Maria Sueli Da Silveira Macedo Moura

Genetics ◽  
1989 ◽  
Vol 122 (1) ◽  
pp. 205-209
Author(s):  
L J Rowland ◽  
D S Robertson ◽  
J Strommer

Abstract We have used a set of Mutator-induced mutants of Bz1 to test whether members of the Mutator (Mu) family of maize transposable elements produce broken chromosomes. From our inability to demonstrate the simultaneous loss of two dominant endosperm markers distal to Mu insertions at Bz1 we conclude that either Mu, unlike many elements of the Ds family, does not induce such breaks, or it does so at a very low frequency.


Sign in / Sign up

Export Citation Format

Share Document