Dear Alex and Vidya,

How about my idea?

Inside the ecmA-lacZ mutant  cells; the ecmA promoter on vector  
deprives the authentic ecmA promoter on genome of its transcription  
factors→The cells cannot differentiate into prestalk cells (Insead,  
the cells may differentiate into prespore cells, which produce DIF) 
→DIF comes→Wild type cells tend to differentiate into PstO.

Reporter gene systems include a fatal risk like 'Uncertainty  
Principle: Indeterminacy Principle by Heisenberg' in the field of  
Quantum mechanics.
The proper fate of a molecule and thus of the cell might be changed  
by your observation with a reporter gene system.

Best wishes,

Yuzuru

On 2010/05/13, at 22:08, Vidya Nanjundiah wrote:

> Dear Alex,
>
> It isn't clear which wild type-mutant mix you have carried out. We  
> have
> seen a preference on the part of wild type cells  to occupy the collar
> region in mixes involving the wild type and the trishanku mutant (see
> Jaiswal et al., Differentiation, Volume 74 Issue 9-10, Pages 596 -  
> 607,
> 2006, "Trishanku, a novel regulator of cell-type stability and
> morphogenesis in Dictyostelium discoideum").
>
> As for wýld type ecmA-lacZ transformants by themselves, do you mean  
> that
> the tip does not show lacZ expression but the collar region does?
>
> cheers
>
> Vidya
>
>
>> Hello everyone,
>>
>> I have been doing alot of studies in chimera, mainly by following
> individual cell types using lacZ reporters.  One of the defects I  
> see is
> very strange - ecmA:lacZ (construct S) in the ecmO collar region. Even
> more strangely is that in a mutant/wild type ecmA:lacZ mix, it is the
> wild type cells that go there!
>>
>> Has anyone ever seen anything like it with things they are working  
>> on or
> know of any papers where a similar phenotype has been seen?  Its a
> difficult search term and i'm not having much luck.
>>
>> Cheers
>> Alex
>>
>
>
>
>
>
> -- 
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