tomm-22
C. elegans
Mitochondrial import receptor subunit TOM22 homolog
What the model saw
Gene: tomm-22 Organism: Caenorhabditis elegans Known functions: Mitochondrial import receptor subunit TOM22 homolog. transmembrane protein transporter activity.
View unredacted entry
Mitochondrial import receptor subunit TOM22 homolog. transmembrane protein transporter activity.
Solver output
TOMM-22 is the C. elegans homolog of TOM22, a core subunit of the translocase of the outer mitochondrial membrane (TOM) complex. This complex is the primary entry gate for nuclear-encoded mitochondrial precursor proteins, and TOM22 serves as both a receptor for cytosolic preproteins and a central organizer of the TOM complex. Proper import of mitochondrial proteins is essential for maintaining mitochondrial proteostasis, respiratory chain assembly, and overall mitochondrial function. Impaired TOM complex activity leads to mitochondrial dysfunction, accumulation of misfolded or mistargeted proteins, and activation of the mitochondrial unfolded protein response (UPRmt). In C. elegans, mild mitochondrial stress via UPRmt activation can paradoxically extend lifespan, but severe loss of TOM22 function would compromise mitochondrial integrity broadly. The net normal function of tomm-22—faithfully importing proteins to sustain mitochondrial homeostasis—supports healthy mitochondrial function and is therefore considered pro-longevity under normal physiological conditions.
GenAge curators classify each gene's normal function as promoting (Pro-Longevity) or opposing (Anti-Longevity) longevity, based on synthesis across studies. Loss-of-function effects can vary from this depending on the manipulation.
Advisor judgment
The model correctly predicted pro_longevity for tomm-22. The mechanistic reasoning is solid - it correctly identifies TOMM-22 as part of the TOM complex involved in mitochondrial protein import, and connects this to mitochondrial proteostasis and UPRmt. The reasoning is somewhat hedged (noting that severe loss would be harmful but mild stress could extend lifespan), but ultimately arrives at the correct conclusion that normal tomm-22 function is pro-longevity. The confidence of 0.62 is appropriately moderate. The mechanism class of "mitochondrial_dysfunction" is a reasonable categorization, though it could be more precisely described as "mitochondrial protein import/proteostasis." Overall a good prediction with sound reasoning.
Raw API responses
solver
{
"reasoning": "TOMM-22 is the C. elegans homolog of TOM22, a core subunit of the translocase of the outer mitochondrial membrane (TOM) complex. This complex is the primary entry gate for nuclear-encoded mitochondrial precursor proteins, and TOM22 serves as both a receptor for cytosolic preproteins and a central organizer of the TOM complex. Proper import of mitochondrial proteins is essential for maintaining mitochondrial proteostasis, respiratory chain assembly, and overall mitochondrial function. Impaired TOM complex activity leads to mitochondrial dysfunction, accumulation of misfolded or mistargeted proteins, and activation of the mitochondrial unfolded protein response (UPRmt). In C. elegans, mild mitochondrial stress via UPRmt activation can paradoxically extend lifespan, but severe loss of TOM22 function would compromise mitochondrial integrity broadly. The net normal function of tomm-22—faithfully importing proteins to sustain mitochondrial homeostasis—supports healthy mitochondrial function and is therefore considered pro-longevity under normal physiological conditions.",
"confidence": 0.62,
"key_pathways": [
"TOM complex / mitochondrial protein import",
"mitochondrial unfolded protein response (UPRmt)",
"mitochondrial proteostasis"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for tomm-22. The mechanistic reasoning is solid - it correctly identifies TOMM-22 as part of the TOM complex involved in mitochondrial protein import, and connects this to mitochondrial proteostasis and UPRmt. The reasoning is somewhat hedged (noting that severe loss would be harmful but mild stress could extend lifespan), but ultimately arrives at the correct conclusion that normal tomm-22 function is pro-longevity. The confidence of 0.62 is appropriately moderate. The mechanism class of \"mitochondrial_dysfunction\" is a reasonable categorization, though it could be more precisely described as \"mitochondrial protein import/proteostasis.\" Overall a good prediction with sound reasoning.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}