In principle much is the same. Whether the transposon is stable should be listed in the description of the mutant population, same goes for the transposon carrying antibiotic selection marker. My guess is, the transposon is self stabilising.

Genotyping will work the same as for T-DNA mutants (unique transposon border primer) and crosses for double mutants can be made as normal. When the transposon is self stabilising (does not contain the transposase) back(crosses) can be made to remove the transposase source.

When the transposon contains the transposase, the mutant phenotype (when detected) could reverse, but footprint mutants upon excision can occur that confer a stable mutant phenotype (in case of frame shift). With PCR/sequencing the exact transposon insert position can be determined and primers designed to check for such footprint/frame shift stable mutations.

Thank you so much for this information, Eric!

Hi  Joanne Ashnest,

I don't know whether you have gone to this site where it explains many things about "Transposon Mutagenesis in Arabidopsis". It is a TAIR site. TAIR, where you purchased these seeds. https://www.arabidopsis.org/info/springer.jsp

Two paragraphs caught my eye:

(1) Two transposable element systems from maize have been widely used in Arabidopsis. They are:

Suppressor-mutator (also called Enhancer) -abbreviated Spm (or En)

Activator/ Dissociation - abbreviated Ac/Ds

(2) Copy number: Spm elements can transpose at a high frequency in Arabidopsis so that, after a few generations, copy number is relatively high. High copy numbers are useful for whole-genome reverse genetics (Das and Martienssen, 1995). By contrast, Ac/Ds systems are easier to control, and more useful for single-copy insertion schemes, such as enhancer trapping.

So, now I have questions:

When you got these seeds, do you know whether they still contain 'transpotase' gene, or transpotase gene has segregated away? If your mutants were generated by Spm or Ac/Ds? If from Spm, and generated multiple gene insertions, then how will you know which mutated gene will responsible for the 'phenotype'?