egsA (araM, yseB; BSU28760; P94527) notes

Provenance of this review

Enzyme activity (well supported)

In vivo role: what is and is not shown

Arabinose operon context

Annotation decisions (summary)

Review pass 2026-11-06: resolving the GO:0006650 question

The earlier plan justified MODIFY GO:0006650 -> GO:0046474 with "G1P feeds
HepGP, which is itself a glycerophospholipid". That reason is not usable: the
same notes record that no egsA-deletion lipidomics ties this enzyme's output to
HepG/Ac-HepG or to the G1P-backbone PG. The action is retained but re-grounded,
on two things that are demonstrated and one structural observation.

  1. The lipid framing is not what this row decides. GO:0046474 is an is_a
    descendant of GO:0006650 (checked: ancestors of GO:0046474 include
    GO:0006650). Both terms assert involvement in glycerophospholipid metabolism;
    the child adds only direction. Keeping the parent would not avoid the
    undemonstrated flux, it would only state it more vaguely. If the flux were the
    problem, the right action would be MARK_AS_OVER_ANNOTATED on the lipid
    wording, not a refinement of it.
  2. Direction is demonstrated without reference to any downstream lipid.
    KM 8.1 uM for DHAP and 16 uM for NADH against 1370 uM for G1P
    [file:BACSU/egsA/egsA-uniprot.txt "KM=8.1 uM for DHAP", "KM=1370 uM for G1P"],
    i.e. about 170-fold against the oxidative side. The enzyme is a reductase that
    forms glycerophosphate.
  3. Comparator check (per CLAUDE.md's NEW/convention guidance, applied here to
    a refinement).     E. coli GpsA (P0A6S7), the stereochemical mirror of EgsA and
    likewise a precursor-supplying NAD(P) glycerophosphate dehydrogenase, carries
    GO:0046474 by IMP from PMID:4591941, PMID:4597451 and PMID:4914567 and by
    IBA, alongside its own precursor term GO:0046167 (QuickGO annotation query,
    2026-11-06). So treating a glycerophosphate dehydrogenase as involved_in
    glycerophospholipid biosynthesis is GO's own convention, not an inference we
    are inventing. GpsA holding both terms is also what shows the ontology gap:
    the G1P enzymes can only hold the lipid term.

Option (b), keeping GO:0006650 until a G1P process term exists, was rejected:
CLAUDE.md forbids ACCEPT/KEEP_AS_NON_CORE while arguing a term is too
general, the term is not as precise as the evidence allows (direction is known),
and an ontology gap is recorded in proposed_new_terms, not by parking a row on
a less specific existing term.

Ontology gap verified: a QuickGO ontology search for "glycerol-1-phosphate"
(2026-11-06) returns only MF terms (GO:0050492, GO:0106357, GO:0106358,
GO:0000121, GO:0120536) and no process term at any level, while GO:0046167
(G3P biosynthesis, under GO:0006072) exists for the other enantiomer. Proposed
sn-glycerol 1-phosphate biosynthetic process under GO:0090407.

Also verified in this pass: neither egsA nor araM occurs anywhere in the
Komazin 2025 full text PMID:40626731, so its screen is silent on EgsA rather
than counter-evidence; the hits are stated as PMID:40626731. The Rieche 2026 second-G1P-route statement is
the authors' reading of Caforio et al. 2018, not new data here
PMID:42286214. Guldan 2008, Sa-Nogueira 1997, Mota 1999, Guldan 2011, Linde 2016,
Palyzova 2022 and the lipid-divide review remain abstract-only in the cache, so
the araM knockout result is still unverified.

2026-11-07 module audit: source scope and complete annotation review

Rechecked all existing annotation rows, references and core functions against the frozen sources. No machine payload, row order or historical NEW assertion was changed; no new annotation was added. The default Falcon attempt failed with HTTP403 and produced no provider report; manual review is documented here instead. Normal PAINT-loss checks returned no IRD/IKR.

The lipid-process claim is now UNDECIDED: kinetic asymmetry does not establish native direction or lipid flux. Broad NAD(P) activity is refined to both existing cofactor-specific children; preferred NAD activity remains core and measured lower-efficiency NADP activity remains non-core. The official author thesis was read separately from the still abstract-only 2008 article; scoped source analysis documents Table10 and the exogenous-G1P bypass in the ΔaraM experiment. The 2026 alternative-G1P statement cites prior engineered E. coli work, not a new B. subtilis pathway.

2026-11-07 PR review follow-up

Kinetic differences between reaction directions do not determine the net cellular flux. This evidence limitation is retained in notes and in the native precursor-flux knowledge gap rather than the standalone biological description.