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Table of Contents
Why Do Genetics
Genetic Terms
More Terms
Basic Molelcular
Biology

More Basic Concepts
Screens
Selections
Mutation Frequency
Chemical Mutagenesis
Frameshift Mutation
DNA Repair
Mutation Summary
Detecting Mutants
Complex Mutation
Insertion Sequences
Compound Transposons
Complex Transposons
Models of
Transposition

Transposition Summary
Mutagenesis in vitro
Effects of Mutations
Complementation
Plasmids and
Conjugation

F Factor
Transformation
Transduction
Generalized
Transduction

Specialized
Transduction

Complementation
Mapping
Two Factor Crosses
Deletion Mapping
Other Mapping Methods
Strain Construction
Inverse Genetics
Gene Isolation
Characterization of
Clones

Sequence Data
General Approaches
Fusions
Supression
Final Summary
Problem Set 1
Problem Set 2


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Models of transposition

©2000 written by Gary Roberts, edited by Timothy Paustian, University of Wisconins-Madison

IV E3. MODELS OF TRANSPOSITION

a. Conservative transposition. Conservative transposition is so named because the copy number of the transposon is conserved during the operation. It involves the transposon physically leaving one replicon and moving to another. The original replicon is apparently destroyed so it is critical that the element transpose to another replicon in the cell. Most elements try to transpose soon after DNA replication because there is then the highest probability that the cell actually contains another replicon. Notice that while conservative transposition does not increase the element's copy number in the cell (at least not initially), it does increase the ratio of transposons to replicons in the cell. This might actually be the reason that Tn's do not repair the site they have left.

The molecular events are illustrated below. The model was developed for Tn5/IS50 and seems to describe the Tn10/IS10. The initial events are (a) double-strand breaks on both sides of the transposon coupled with staggered single-strand breaks in the target replicon (the staggers are the cause of the small duplications shown in figure 18). (b) The ends of the transposon are then ligated to the single-strand segments in the target DNA. Finally, the gaps in the target molecule are filled in.

b. Bi-directional replicative transposition. This model, shown on the next page, differs from the previous one in several important ways: the transposon increases its copy-number in the cell directly and the donor molecule is not destroyed. It apparently explains the mechanism employed by Tn3 and Mu. It involves .

  1. Single-strand breaks in the target DNA and on either side of the transposon

  2. Ligation of ends as shown to produce a complicated hybrid molecule (not shown)

  3. bi-directional replication through the element with subsequent ligation

  4. This results in production of a single replicon where the donor replicon is flanked by 2 copies of the transposon and fused to the target replicon.

  5. A replication event "resolves" this to the finished product

In the case of each of these models it should be realized that they are in fact only models and definitive proof of these mechanisms is still lacking, though the recent development of in vitrotransposition systems is extremely promising.

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