Repeated activities in pathway

[kimrutherford]

There are a bunch of repeats chunks in this pathway. Is that expected? Why is SPAC922.06 in the first chunk but not the others?

https://www.pombase.org/gocam/gene/678073a900002931/SPBC887.13c/cem1

[ValWood]

Yep this is representing fatty acid elongation...

We could add inputs and outputs to clarify

[kimrutherford]

We could add inputs and outputs to clarify

Yep, that probably would help.

What mechanism stops the elongation continuing forever?

[ValWood]

CHAT-GPT
Fatty acid elongation is prevented from continuing by product inhibition and substrate specificity at key enzymatic steps. The primary mechanisms include:

Thioesterase Activity – In de novo fatty acid synthesis (occurring in the cytoplasm via fatty acid synthase, FAS), thioesterase enzymes (such as TE in mammals) recognize fatty acyl chains of specific lengths (typically palmitate, C16:0) and hydrolyze them from the acyl carrier protein (ACP), terminating elongation.

Substrate Specificity of Elongation Enzymes – In the endoplasmic reticulum (ER), fatty acid elongation occurs via elongase (ELOVL) enzymes, which have substrate preferences for certain chain lengths. Once a fatty acid reaches an unsuitable length for a given ELOVL enzyme, elongation ceases.

Malonyl-CoA Availability – The elongation process depends on the availability of malonyl-CoA, which donates two-carbon units. If malonyl-CoA levels drop, elongation slows or stops.

Feedback Inhibition – Accumulation of long-chain fatty acids or their derivatives (e.g., acyl-CoA, phospholipids) can inhibit enzymes involved in fatty acid synthesis and elongation, preventing excessive elongation.

Compartmentalization and Competition – Fatty acids may be diverted into β-oxidation, desaturation, or incorporation into lipids, reducing their availability for further elongation.