On 2016 Oct 14, Daniel Jarosz commented:

None

On 2016 Oct 14, Daniel Jarosz commented:

We considered this possibility extensively, and expected to find it commonly. However, we did not observe a change protein levels for the hit proteins that we checked (see supplement), and it seems unlikely that such feedback mechanisms would be transmissible to other cells through protein alone, so strongly sensitive to transient inhibition, or stable over hundreds of generations, through freeze/thaw etc. Investigating whether any of the remaining phenotypic states that we did not test in this way could arise from feedback mechanisms like those described in this comment stands as a goalpost for our future studies.

On 2016 Oct 12, Peter Ellis commented:

The authors note that many of the proteins identified in this screen were transcription factors and RNA-binding proteins. The paper does not report whether they checked the mRNA and/or protein expression levels of the endogenous gene copy before and after transgenic overexpression of a given gene. In cases where a transcription factor promotes its own expression, or an RNA-binding protein promotes the translation of its own transcript, there is an obvious feedback mechanism through which the memory could be maintained.

On 2016 Oct 12, Peter Ellis commented:

The authors note that many of the proteins identified in this screen were transcription factors and RNA-binding proteins. The paper does not report whether they checked the mRNA and/or protein expression levels of the endogenous gene copy before and after transgenic overexpression of a given gene. In cases where a transcription factor promotes its own expression, or an RNA-binding protein promotes the translation of its own transcript, there is an obvious feedback mechanism through which the memory could be maintained.

On 2016 Oct 14, Daniel Jarosz commented:

None