DMRT1 is reviewed as one nuclear, sequence-specific transcription factor. Its activation and repression activities depend on the target and cellular context. The review preserves all 38 imported annotation records and the three official predicted human products. No new annotation is proposed. Experimental species, constructs and developmental stages below delimit the evidence; they are not reasons to dismiss a valid ortholog inference.
Murphy et al., PMID:26005864 directly studied human DMRT1. The structural preparation comprised residues 67–136, whereas additional full-length in-vitro translation, glutaraldehyde crosslinking and gel-shift experiments demonstrated DNA-dependent association with different stoichiometries. Adult human testis ChIP-seq supports chromatin occupancy. The ChIP-exo analysis of inferred stoichiometries was mouse; it is not a direct measurement at every human site. The original Results and Methods were read from the genuine full cache. The one short quotation is in the core; reference-only support elsewhere avoids repeating it.
PMID:17605809(https://pmc.ncbi.nlm.nih.gov/articles/PMC1931443/) used mouse protein for biochemical experiments and a human DMRT1–VP16 fusion for a reporter experiment. The unmodified human protein did not show the same activation in that reporter context. Accordingly, activation is supported additionally by the inducible human DMRT1 experiments in PMID:37709822(https://pubmed.ncbi.nlm.nih.gov/37709822/), especially Figure 6h–i: DAZL cis-regulatory genomic-peak luciferase reporters respond to inducibly expressed human DMRT1 in HEK293 cells. The three tested peaks are not all promoters. Motif deletions were included, but the main text and legend alone do not establish their directional effect; no figure-pixel or source-data read is claimed. The latter paper's engineered human germ-cell model also shows mitotic arrest during a prospermatogonial transition. This does not contradict a positive proliferative role in mouse spermatogonia at another stage. The authors explicitly caution that high transgene levels and imperfect temporal control may accelerate arrest within 4–8 days; dose and induction schedule also limit comparison to endogenous physiology. Full original Methods and Results were read for both sources.
PMID:20951351(https://pmc.ncbi.nlm.nih.gov/articles/PMC2996490/) combines mouse cell-specific deletion, promoter occupancy and expression assays. Stra8 repression and Sohlh1 activation support opposite regulatory directions within one activity. The RARE reporter response is indirect: the paper did not detect DMRT1 binding to that reporter. The negative meiotic-regulation annotation denotes transcriptional control of entry, not chromosome segregation by DMRT1. Short exact source anchors occur once each in the YAML; duplicate source rows retain reference-only support. The dated notes appendix identifies the added excerpts and their assay limits.
The main text of PMID:28473536(https://pubmed.ncbi.nlm.nih.gov/28473536/) describes human transcription-factor methyl-SELEX and its construct and selection procedures. The precise DMRT1 supplementary construct/measurement row was not recovered. The original experimentally curated sequence-specific binding claim is retained, with a gene-level refinement supported independently by PMID:26005864 and promoter evidence. No DMRT1-specific methylation preference or exact current-product construct is inferred from the general Methods.
The checked QuickGO typed paths place GO:0000978 below the broader imported regulatory, cis-regulatory, double-stranded and sequence-specific DNA-binding terms. The refinements preserve the biological claim; they do not rewrite what the original isolated assay measured. The positive and negative RNA polymerase II process terms are descendants of the two broad transcription-regulation terms. These existing terms are used as replacements, not added as duplicate new annotations.
PMID:11040213(https://pubmed.ncbi.nlm.nih.gov/11040213/) directly examines mouse null gonads, postnatal Sertoli/germ-cell differentiation and nuclear staining. The actual original includes cell morphology and postnatal defects. PMID:17540358(https://pubmed.ncbi.nlm.nih.gov/17540358/) resolves cell-autonomous and non-autonomous requirements by conditional targeting. Its genuine cache carries full_text_available: true and an HTML extraction label, but its retained body lacks complete Results and Methods. Only its abstract and available discussion are claimed as read; failed original recovery is recorded. The earlier complete null-study evidence independently supports the differentiation interpretation.
PMID:21775990(https://pmc.ncbi.nlm.nih.gov/articles/PMC3150961/) remains abstract-only in the normal cache. Its complete original PMC HTML was recovered independently and selected Results and Methods were read, including conditional and adult deletion, FOXL2/SOX9 responses and promoter occupancy. These mouse experiments concern postnatal male-fate maintenance. The linked erratum corrects two figure labels; it is not a retraction. The original is not described as evidence that DMRT1 is the fetal mammalian SRY-like initiating switch.
PMID:30272154(https://pubmed.ncbi.nlm.nih.gov/30272154/) supplies human fetal-testis knockdown evidence. Partial first-trimester depletion did not prevent testis formation; second-trimester treatment disrupted cords and produced focal dysgenesis. These findings do not prove first-trimester dispensability, complete female conversion, or every detailed mouse mechanism. The induced human-protein reporter evidence and these human tissue findings complement, rather than replace, the curated mouse inferences.
PMID:21621532(https://pubmed.ncbi.nlm.nih.gov/21621532/) supplies positive mouse fetal-ovary evidence for transient cytoplasmic localization: nuclear staining at E13.5 shifts to the cytoplasm at E14.5 before loss. Its positive Stra8 context differs from negative regulation in male spermatogonia. The cytoplasmic annotation is retained as contextual; no independent cytoplasmic activity is invented.
PMID:22899867(https://pubmed.ncbi.nlm.nih.gov/22899867/) is a human gonadal immunohistochemistry source, available here only as an abstract despite attempted full-original recovery. Its curator-backed nuclear annotation is supported independently by human testis chromatin occupancy. Specific antibody controls not accessed in the original are not supplied from assumption. PMID:23473982(https://pubmed.ncbi.nlm.nih.gov/23473982/) provides the mouse chromatin-binding source; its cache is abstract-only, with selected indexed original ChIP/gel-shift passages recovered separately. The human chromatin conclusion does not depend on an unclaimed complete read of that paper.
The exact mouse donor is UniProt Q9QZ59, and the signaling donor is rat Q925A6. Saved QuickGO source records connect the imported terms to actual experimental PMIDs. PAINT assigns the relevant functions at PANTHER:PTN000960547; the current family tree places human DMRT1 beneath it. Negative assertions at PTN000268760 are on another branch. The nuclear assertion's use of the target itself as experimental grounding is expected and is not circularity. No donor-count argument is used.
Actual ARBA rules and target InterPro/FunFam matches support the broad DNA-binding predictions. ARBA00027852 group 46 matches the target FunFam and Homo taxon. ARBA00026779 groups 3 and 33 match domain/family or FunFam conditions with Euarchontoglires. Current InterPro2GO mappings for IPR001275, IPR026607 and IPR036407 agree with DNA recognition, transcription regulation and/or nucleus. These predictions are refined using target biology, not rejected as computational evidence.
The unresolved row is rat-derived GO:0035556 intracellular signal transduction, tracing to PMID:11181532(https://pmc.ncbi.nlm.nih.gov/articles/PMC1496887/). The accessible abstract and indexed passages show FSH/cAMP/PKA and phorbol ester regulation of Dmrt1 mRNA. Complete original retrieval was blocked by access challenges. Regulation of a gene by signaling does not alone identify its protein as performing a signal-relay step. The review therefore uses UNDECIDED, preserving the experimental source and avoiding a categorical misattribution or removal.
UniProt Q9Y5R6 and independently fetched official FASTAs establish predicted DMRT1a at 373 residues, DMRT1b at 275, and DMRT1c at 175; this sequence reconstruction does not demonstrate production or function of every protein in vivo. The latter replaces sequence beginning at residue 120. Although the annotated DM feature at 72–118 remains, the experimentally characterized 67–136 recognition region includes R123 beyond that feature boundary. The short product therefore cannot be declared functionally equivalent from domain retention alone; inactivity is also unproven. PMID:16617334(https://pubmed.ncbi.nlm.nih.gov/16617334/) reports transcript diversity, but its available abstract does not establish equivalent biochemical function of the three products.
Publications and other machine caches are preserved exactly. Full-original recovery outside a cache is identified above rather than retroactively changing its flags. Normal recovery of PMID:20616082 failed with HTTP 429; it is documented as a source in the donor provenance but is not fabricated as a local publication or used for an unsupported original-method claim. The separate automated research attempt failed authentication/quota checks; all biological assessments above come from the explicitly identified sources.