title: DNM2 source and assay guide
gene: DNM2
annotation_scope:
imported_annotations: 171
new_annotations: 0

DNM2 source and assay guide

This guide locates the evidence supporting the review. Reference assessments distinguish selected original passages from abstract-only access. Machine cache variants retain their original text and flags; the effective shared-cache selection is described below. Primary citations, rather than this guide, support the biological assertions.

Motor and membrane-remodeling evidence

The core uses GO:0061791 GTPase motor activity. PH-domain phospholipid binding and partner recruitment are mechanisms within this motor unit. Existing process coverage includes scission, receptor-mediated endocytosis, macroautophagy and actin-bundle organization. No additional process annotation is manufactured from necessity alone.

Current ontology and comparator check (2026-10-18 UTC)

The is_a-only QuickGO ancestry query places GTPase motor activity below GTPase activity. The definition requires mechanical activity driven by GTP hydrolysis. DNM2 human hydrolysis/fission and membrane-polymer evidence supports that refinement; rat and human assays retain their source boundaries. The narrower GO:1990606 definition additionally specifies twisting, which is not assumed from every fission assay.

The following complete current human queries used the verified UniProt accession and the indicated term plus is_a/part_of descendants. Counts are records, not independent experiments:

Reproduce the DNM2 motor query; substitute each accession and GO:0003924 for the paired comparison. The complete all-taxon motor query returns four PomBase records on this date: msp1/P87320 (TAS) and fzo1/Q9USY7 (ISM) to GO:0061791, plus dnm1/Q09748 and vps1/Q9URZ5 (both TAS) to GO:1990606. Official identities confirm dynamin-family comparators. These records demonstrate real use of the motor branch in this protein family while preserving the observed absence in the human records. The query is not itself biochemical evidence for DNM2, and human non-use is not claimed to be a curator mistake.

The two autophagy sources resolve different stages. The 2020 accepted manuscript, Results section on DNM2-mutant accumulation and Figure 5D–E, reports unchanged numbers of open phagophores but accumulation of completed autophagosomes and fewer autolysosomes. Live imaging shows failure to detach LC3 vesicles from RAB11A-positive tubules. The adjacent ATG9A/ATG16L1 and SNX18 controls explicitly distinguish this release step from early ATG9A trafficking. Row 121 is therefore refined to GO:0016236 macroautophagy, without assigning double-membrane formation or closure. The 2018 original, Figures 3/4 and WT/W38K experiments, independently supports DNM2-dependent ATG9A carrier generation and ATG16L1 delivery for GO:0000045 autophagosome assembly in row 122. The core uses macroautophagy once and describes both stages. Neither route is claimed to supply every autophagosome.

The current GO:0097352 maturation definition specifies removal of PI3P and Atg8/LC3 after closure, which was not established here. GO:0061906 localization concerns transport to or maintenance at a cellular location; detachment alone does not demonstrate that process. GO:1905037 organization concerns constituent assembly, arrangement or disassembly, which would still infer an organizational step from the 2020 release endpoint. These terms are not substituted merely because their names sound like later stages.

Interactions and repeated partners

The executable interaction analysis provides public dataset URLs, exact snapshot digests, literal MITAB fields, AP-MS edge identifiers and OpenCell accession groups. It separates all incident records from the subset selected by the imported source annotations. A missing MITAB match is an unresolved database join, not a negative experiment.

PMID:16696976 is especially qualified: MINT identifies PRD/SH3 fragments, but some original protein taxids were unspecified and human homolog accessions were supplied by curation. This does not authenticate a human recombinant template. In PMID:22022388, a sequenced human SH-SY5Y-derived clone supports NPRAP/CTNND2 association; its historical isoform label is not automatically a modern UniProt product ID.

Localization, processes and propagation

HPA DNM2 localization supports cytosol and Golgi. Selected membrane pools are supported by the original trafficking studies. Cytoplasm replacements retain cytosol and recycling-endosome membrane. Clathrin-coated pits are plasma-membrane invaginations outside the defined cytoplasm and remain in their own positive rows/core. The cytoskeleton mapping is refined to microtubule; focal adhesions are junctions and retain their separate positive detection. This is a source-specific compartment distinction, not exhaustive distribution in every cited cell. Urinary-vesicle proteomics and focal-adhesion proteomics retain their contextual detections despite incomplete recovery of the target supplementary rows.

The PANTHER family PTHR11566 path to DNM2 contains all eight literal PAINT ancestral assertions. PTN000170013 grounds the GTPase/cytoplasm/microtubule placements; PTN008520579 the plasma-membrane placement; PTN000902093 the synaptic-vesicle-budding/synapse placements; PTN002611550 receptor internalization. These are ancestral placements, not pairwise transfers or donor-count scores.

PMID:11076973(https://pubmed.ncbi.nlm.nih.gov/11076973/) provides Drosophila affinity/cosedimentation context. PMID:21210813(https://pubmed.ncbi.nlm.nih.gov/21210813/) directly examines rat neuronal growth cones, domain perturbations and adhesions, with separate HeLa antibody controls. Neither is a purified human neuronal assay. PMID:21195118(https://pubmed.ncbi.nlm.nih.gov/21195118/) supports mitotic phosphorylation and cytokinesis, which does not by itself settle the historical G2/M transition assertion.

The Reactome sources can be inspected at their exact event pages, including dynamin-mediated scission R-HSA-8868661, Golgi scission R-HSA-421835, Golgi-to-lysosome scission R-HSA-432707, BAR-domain recruitment R-HSA-8868236, and NOSTRIN trafficking R-HSA-203625. The review preserves each cited event and nested target assignment. A rate-limited API endpoint is not treated as a biological negative. ARBA condition reconstruction remains incomplete and is identified as such in the propagation review.

Products and source access

UniProt P50570 defines five official products, with lengths 870, 866, 866, 870 and 869 residues. The alternative sequence features are preserved exactly. Historical aa/ab/ba/bb and named disease constructs require sequence reconciliation before product-specific conclusions; similar lengths or a human cell host are insufficient. No product is declared universally inactive.

The table below reports effective publication-cache availability, not a claim that every paragraph of a full cache was read. Additional independently recovered original scope is stated above and in each reference assessment.

Positive generic binding without an evidenced finer class remains non-core under the explicit ClinGen project instruction. The biological review is independent of provider availability; failed provider attempts did not produce a substitute provider-named report. The two inherited core quotes remain unchanged. Three additional short assay excerpts appear once each in YAML rows 119, 122 and 156; this guide adds no publication quotations.

Shared publication reconciliation

The existing DNM1 source versions are reused for PMID:15703209 (full text) and PMID:17257598 (abstract only). The initial DNM2 fetch produced the opposite availability pattern; those genuine variants were retained as provenance. In particular, the detailed Myo1E/DNM2 evidence from PMID:17257598 was actually read in the independently fetched full original even though the shared publication cache is abstract-only. PMID:18425118 retains the existing full cache, while this review read only its abstract. No source text was spliced or rewritten to change availability.