It makes sense. You may be the first to demonstrate directly that exposure to  stress by UPR, affects elongation. I wonder however whether you are considering cases in which the two events occur in the same cell. Elongation may not occur in the same cell type than ER stress is occurring. I am thinking in ER stress in neurons in which I would think that elongation is not taking place.

Thank you for you answer.

As I work with yeast I was wondering about it, actually. I was not thinking about mammalian cells but you are right.. different cells may lead to different responses.

It seems to highly depend on the cell context. Fatty acid elongation occurs robustly in the steroid-producing cells in ovary, testis, and adrenal gland cortex. These cells are considered to have resistance to UPR due to the FA elongation. Rather that, these cells with high amount of smooth ER are likely to activate UPR under the presence of mis-folding proteins.  

Yes, your question is interesting and worth investigating. However, I am unable to comprehend what exactly do you mean by ER stress? I completely agree that membranes are assembled by ER. Accordingly, length and the degree of unsaturation of fatty acids of membrane lipids are also regulated by ER. If you allow living beings or their cells to get adapted to various temperatures, you can see variation in the degree of unsaturation of fatty acids or may be even their length. The organism or the cell that has potential to tolerate low temperatures invariably show higher degree of unsaturation for regulating membrane fluidity. As fatty acid chain length also contributes significantly towards membrane fluidity, you can expect significant change in regulation of fatty acid length by ER. For me, ER of cells or living beings exposed to stress (for in stance low temperature or freezing stress) show significant variation in its functioning. I strongly believe that your idea is brilliant and you must investigate into this aspect.

This is just my view.

Thank you for your answers.

P. Pardha-Saradhi, indeed cells can adapt in various ways which makes it difficult to tackle the question. The scenario I was picturing would be constitutive ER stress due to (also constitutive) amino acid exchanges in random proteins.

That means you are referring to a situation, where cell metabolic activities requiring rapid protein  synthesis  (especially those guided/processed by ER) and membrane synthesis etc. are extremely active. ER besides helping in apt folding and post/co-translational modifications of proteins, also picks up & takes care of improper (in terms of improper amino acid sequence or improper folding etc.) proteins/polypeptides..

Coming back to your key question, I have not come across any study which links ER stress with fatty acid elongation. However, it is worth investigating into. If you find a link, one day I may quote your work to our students (I believe that membrane is key of life and hence, I keep on educating myself on various aspects of membrane biology) .

Good Luck

You may find :-

http://www.ncbi.nlm.nih.gov/pubmed/18793169

http://www.ncbi.nlm.nih.gov/pubmed/16492686

relevant.

Thank you Shivani for good reviews on fatty acid elongation in relation to ER stress.

thank you for the links. The idea behind ER stress caused by FA supplementation is that each organelle has a different PL composition and the exogenus FA are inserted into PL that end up in ER membranes, among others. This disturbs their original composition and hence their function. My question was about how first causing ER stress would affect FA after.