The complete OpenScientist report
was read after the full 67-row review. GO:0044351 remains UNDECIDED. The report
reference is DISPUTED, and no duplicate report was requested.
Useful findings include the distinction between pan-Ras activity reporters and
RasC-specific localization, established RasG/RasS/RasB effectors in
macropinocytosis, and RasC's TORC2/PKB and adenylyl-cyclase roles. RasC failure to
substitute for RasG in suspension growth and cytokinesis (PMID:20833893) is
relevant functional-divergence evidence, but suspension growth is a composite
readout and does not by itself determine every direct/regulatory role in uptake.
The report states “there is no such deletion-uptake dataset in evidence either
way.” This omits PMID:15878331, already cited in the gene review. Its primary
abstract explicitly reports larger rasC-null cells and states: “These increases
were associated with increased liquid phase endocytosis.” It also describes
relatively normal cytokinesis and unchanged division rate. This is a real RasC
perturbation/uptake dataset, not a hypothetical scenario supplied in the prompt.
The cached article remains abstract-only, so the precise normalization and cup
mechanism cannot be adjudicated from it alone.
An increased uptake phenotype is compatible with an inhibitory role,
compensatory signaling or a change in cell size; it is not automatic proof that
RasC is absent from the process. Likewise, identification of other positive Ras
effectors does not establish exclusive process membership. The report's
automatic classification of any RasC uptake phenotype as secondary goes beyond
its evidence. The direct cytokinesis comparison remains a separate decision;
it is not simply copied to macropinocytosis.
The PAINT table was re-read: the macropinocytosis IBD is at PTN001177391 in
PTHR24070, with experimental Dictyostelium descendant evidence. This is an
ancestral functional assertion, not a ~66% pairwise similarity transfer. The
report's sequence-identity matrix has no delivered executable alignment/output
artifact and cannot establish the location of functional divergence on that
tree. No sequence result is adopted as independent evidence here.
Human follow-up should reconcile the actual fluid-uptake measurements,
normalization for cell size, paralog compensation and any RasC-specific
macropinocytic-cup function before asserting a target loss. The report does not
resolve that question.