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Subunit interactions in the mariner transposase

A R Lohe1, D T Sullivan, D L Hartl

  • 1Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA.

Genetics
|November 1, 1996
PubMed
Summary
This summary is machine-generated.

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Mos1 transposase, a DNA-cutting enzyme, may function as a multi-subunit complex. Evidence suggests that interactions between Mos1 subunits regulate mariner transposition activity.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • The Mos1 transposase is a key enzyme in the transposition of the mariner genetic element.
  • Mos1 belongs to the D,D(35)E superfamily, characterized by a conserved D,D(34)D motif.
  • The oligomeric state of eukaryotic transposases, including Mos1, has not been definitively established.

Purpose of the Study:

  • To investigate whether the Mos1 transposase functions as a multimeric complex.
  • To explore the potential role of subunit interactions in the regulation of mariner transposition.

Main Methods:

  • Negative complementation assays using EMS-induced Mos1 mutations, including the G292R catalytic domain mutation.
  • Yeast two-hybrid system to detect Mos1 subunit interactions.

Related Experiment Videos

  • Analysis of Mos1 overproduction effects on target element excision.

    • Main Results:

    • Negative complementation was observed with the G292R mutation and two other EMS mutations, indicating interference with wild-type Mos1 function.
    • The yeast two-hybrid system provided evidence for Mos1 subunit interactions.
    • Overproduction of Mos1 subunits inhibited target element excision, suggesting autoregulation or formation of inactive oligomers.

    Conclusions:

    • The findings support the hypothesis that Mos1 transposase functions in a multimeric form.
    • Subunit interactions and oligomerization likely play a significant role in regulating mariner transposition.
    • Negative complementation and overproduction effects may represent mechanisms of autoregulatory feedback for transposition control.