Component

Human phosphatidylserine decarboxylase / PISD

Context-specific entity; species, compartment and exposure are stated on each claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Human PISD converts phosphatidylserine to phosphatidylethanolamine in the inner mitochondrial membrane; patient fibroblasts with PISD variants showed reduced conversion.

    Human phosphatidylserine decarboxylase / PISD → Phosphatidylethanolamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human family genetics and fibroblast lipid-conversion measurements.
    limitations
    This pathway uses membrane-bound phosphatidylserine, not free serine as the direct PISD substrate.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    A serine-derived lipid feeds another lipid needed inside mitochondria.
    primary_references
    PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 422–428

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human family genetics and fibroblast lipid-conversion measurements. · source_derived_draft · unverified_draft

    ## l-serine-pisd-decarboxylation A serine-derived lipid feeds another lipid needed inside mitochondria. Human PISD converts phosphatidylserine to phosphatidylethanolamine in the inner mitochondrial membrane; patient fibroblasts with PISD variants showed reduced conversion. Model: Human family genetics and fibroblast lipid-conversion measurements. Limitations: This pathway uses membrane-bound phosphatidylserine, not free serine as the direct PISD substrate. Evidence access: Primary abstract PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    Complete structured claim and evidence

  2. PISD patient fibroblasts had fragmented mitochondria, enlarged lysosomes and reduced maximal oxygen consumption; one variant impaired the enzyme autocatalytic processing required for activity.

    Human phosphatidylserine decarboxylase / PISD → Mitochondrial function in PISD patient fibroblasts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Two affected sisters, patient fibroblasts and functional variant characterization.
    limitations
    The other allele produced an alternative splice product; different molecular defects remain distinct.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    A downstream processing defect can persist despite precursor availability.
    primary_references
    PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 430–436

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Two affected sisters, patient fibroblasts and functional variant characterization. · source_derived_draft · unverified_draft

    ## l-serine-pisd-failure A downstream processing defect can persist despite precursor availability. PISD patient fibroblasts had fragmented mitochondria, enlarged lysosomes and reduced maximal oxygen consumption; one variant impaired the enzyme autocatalytic processing required for activity. Model: Two affected sisters, patient fibroblasts and functional variant characterization. Limitations: The other allele produced an alternative splice product; different molecular defects remain distinct. Evidence access: Primary abstract PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Lyso-PE treatment and genetic complementation restored mitochondrial and lysosomal morphology in PISD patient fibroblasts.

    Lysophosphatidylethanolamine → Organelle morphology in PISD patient fibroblasts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human patient fibroblast rescue experiments.
    limitations
    This is not evidence that oral serine or phosphatidylserine corrects PISD disease.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    Supplying a downstream lipid can bypass a specific defect in culture.
    primary_references
    PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 438–444

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human patient fibroblast rescue experiments. · source_derived_draft · unverified_draft

    ## l-serine-pisd-lipid-rescue Supplying a downstream lipid can bypass a specific defect in culture. Lyso-PE treatment and genetic complementation restored mitochondrial and lysosomal morphology in PISD patient fibroblasts. Model: Human patient fibroblast rescue experiments. Limitations: This is not evidence that oral serine or phosphatidylserine corrects PISD disease. Evidence access: Primary abstract PISD is a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30858161/ · DOI 10.26508/lsa.201900353
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards