Affinage

PRDM9

Histone-lysine N-methyltransferase PRDM9 · UniProt Q9NQV7

Length
894 aa
Mass
103.4 kDa
Annotated
2026-06-10
100 papers in source corpus 38 papers cited in narrative 36 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 10/10 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRDM9 is a meiosis-specific zinc finger histone methyltransferase that determines the genomic positions of meiotic recombination hotspots, coupling sequence-specific DNA recognition to histone methylation and ultimately to double-strand break (DSB) formation and homolog synapsis (PMID:20044539, PMID:20044541, PMID:20044538, PMID:29478809). Its tandem C2H2 zinc finger array binds specific hotspot motifs with nanomolar affinity and slow dissociation, requiring the full array for binding; the array also mediates assembly into a trimer in which only one zinc finger module contacts DNA while the other two maintain the oligomer (PMID:20044539, PMID:20044541, PMID:20044538, PMID:28155083, PMID:31308055, PMID:23618393). Allele-specific crystal structures of zinc fingers bound to cognate hotspot DNA define the rules of base recognition and explain differential binding affinity and allelic dominance among human PRDM9 variants (PMID:26833727, PMID:28801461). Through its PR/SET domain PRDM9 catalyzes mono-, di-, and trimethylation of H3K4 and also trimethylates H3K36, depositing both marks on the same flanking nucleosomes at hotspots in a manner dependent on its catalytic activity; pre-SET and post-SET domains impose an autoinhibitory conformational switch (PMID:24095733, PMID:24634223, PMID:27362481, PMID:29478809). To gain chromatin access, PRDM9 partners with the SNF2-like remodeler HELLS to form a pioneer complex that opens chromatin and reorganizes nucleosomes into a symmetric depleted region centered on the binding motif, where DSBs are introduced (PMID:24604780, PMID:32001511, PMID:33047671). The dual H3K4me3/H3K36me3 signature is read by ZCWPW1, which is required for DSB repair and synapsis, and the methylation marks designate sites from which a subset is selected for SPO11-dependent breakage (PMID:29478809, PMID:32374261, PMID:32744506). PRDM9's KRAB domain organizes a protein complex—including CXXC1, EWSR1, EHMT2, CDYL, FUS/TLS, and the meiotic cohesins STAG3 and REC8—that tethers marked hotspots to the chromosome axis and links hotspot designation to the DSB machinery; the KRAB domain is required for full meiotic function in vivo (PMID:27932493, PMID:28527011, PMID:30853435, PMID:33175657, PMID:36967403). The degree of symmetric PRDM9 binding on both homologs governs successful synapsis and fertility, and humanizing the mouse zinc finger array repositions hotspots and rescues hybrid sterility (PMID:26840484). PRDM9 deficiency causes sterility in both sexes in mice, and functional PRDM9 variants that impair methyltransferase activity cause premature ovarian insufficiency in humans (PMID:20044538, PMID:20044539, PMID:20044541, PMID:34257419). Beyond its canonical meiotic role, PRDM9 methylates the nonhistone substrate CTNNBL1 and drives H3K4me3-dependent transcriptional programs during somatic brown adipocyte differentiation (PMID:36972790, PMID:37579296).

Mechanistic history

Synthesis pass · year-by-year structured walk · 32 steps
  1. 2009 High

    Establishing the molecular determinant of recombination hotspot positioning resolved how hotspot locations are specified, identifying PRDM9 zinc finger recognition of a specific DNA motif as the trigger.

    Evidence In vitro DNA binding assays plus genetic association of zinc finger variants with hotspot usage across human and mouse

    PMID:20044538 PMID:20044539 PMID:20044541

    Open questions at the time
    • Did not show how binding leads to break formation
    • Did not define the downstream protein complex
  2. 2009 High

    Identifying PRDM9 as an essential meiotic H3K4 trimethyltransferase linked hotspot designation to a chromatin-modifying enzymatic activity required for fertility.

    Evidence Prdm9-null mouse knockout with sterility phenotype and enzymatic H3K4me3 characterization

    PMID:20044538 PMID:20044539 PMID:20044541

    Open questions at the time
    • Did not establish whether methylation is required for DSB formation
    • Second substrate H3K36 not yet known
  3. 2011 High

    Demonstrating that zinc finger specificity dictates H3K4me3 placement and crossover distribution causally connected DNA binding to chromatin marking and recombination outcome.

    Evidence Transgenic mice with modified zinc fingers, in vitro binding, ChIP for H3K4me3, and genetic crossover mapping

    PMID:22028627

    Open questions at the time
    • Mechanism of break formation downstream of marking unresolved
  4. 2013 High

    Crystal structures of the PR/SET domain defined the substrate-binding and autoinhibition mechanism, explaining how PRDM9 achieves multistate H3K4 methylation.

    Evidence X-ray crystallography of active and autoinhibited states with in vitro methyltransferase assays

    PMID:24095733

    Open questions at the time
    • Did not address H3K36 activity
    • In vivo relevance of autoinhibition not tested
  5. 2014 High

    Identifying H3K36 as a second substrate expanded the chromatin signature PRDM9 deposits, foreshadowing a combinatorial mark.

    Evidence In vitro kinetic methyltransferase assays and overexpression in HEK293 cells with histone mark western blotting

    PMID:24634223

    Open questions at the time
    • In vivo co-deposition on the same nucleosomes not yet shown
  6. 2014 Medium

    Systematic biochemical mapping established that the full zinc finger array is required for binding and that in vitro affinity parallels biological activity, defining the binding-specificity code.

    Evidence In vitro EMSA with systematic mutagenesis across hotspot sequences and PRDM9 alleles

    PMID:23618393

    Open questions at the time
    • Did not resolve oligomeric state of the bound protein
  7. 2014 Medium

    Active-site mutagenesis (C321P) pinpointed the catalytic residue and revealed additional histone substrates, providing the tool used in later loss-of-catalysis studies.

    Evidence Site-directed mutagenesis and methyltransferase assays on recombinant histone octamers

    PMID:24785241

    Open questions at the time
    • Single in vitro study
    • Physiological role of additional substrates untested
  8. 2014 High

    Showing that PRDM9 reorganizes nucleosomes into a symmetric depleted region centered on its motif explained how break sites are spatially positioned relative to binding.

    Evidence Genome-wide ChIP-seq, MNase-seq, and genetic crossover boundary analysis in two zinc-finger-divergent mouse strains

    PMID:24604780

    Open questions at the time
    • Remodeling machinery responsible for nucleosome reorganization not identified
  9. 2015 Medium

    Defining the narrow developmental window of PRDM9 nuclear localization and its dispensability for cohesin axis incorporation clarified when and where PRDM9 acts in meiotic prophase.

    Evidence Stage-specific immunofluorescence and RAD51 focus quantification in wild-type versus Prdm9-null germ cells

    PMID:25894966

    Open questions at the time
    • Did not define the protein partners mediating axis tethering
  10. 2015 Medium

    Demonstrating allelic competition and dosage sensitivity showed that PRDM9 heteromers compete, with the stronger allele suppressing the weaker, shaping hotspot usage in heterozygotes.

    Evidence Cell-culture co-expression, ChIP-seq for H3K4me3 in heterozygous/hemizygous mice, and crossover analysis

    PMID:26368021

    Open questions at the time
    • Structural basis of allelic dominance not resolved here
    • Trimer stoichiometry not yet defined
  11. 2016 High

    Allele-specific co-crystal structures established the molecular grammar of base recognition and explained differential affinity and allele dominance.

    Evidence X-ray co-crystallography of PRDM9A and PRDM9C zinc fingers with cognate hotspot DNA plus binding affinity measurements

    PMID:26833727 PMID:28801461

    Open questions at the time
    • Did not address how oligomerization affects DNA engagement
  12. 2016 High

    In vivo confirmation that PRDM9 places both H3K4me3 and H3K36me3 on the same nucleosomes at hotspots defined the combinatorial mark distinguishing hotspots from other genomic sites.

    Evidence ChIP-seq in wild-type and Prdm9-null spermatocytes with dual-mark co-detection and in vitro assays

    PMID:27362481

    Open questions at the time
    • Reader of the dual mark not yet identified
  13. 2016 High

    Humanizing the mouse zinc finger array repositioned hotspots and rescued hybrid sterility, and identified symmetric binding on both homologs as the determinant of fertility.

    Evidence Humanized knock-in mouse with PRDM9 ChIP-seq, SSDS DSB mapping, and hybrid fertility assays

    PMID:26840484

    Open questions at the time
    • Mechanism by which binding symmetry promotes repair/synapsis not resolved
  14. 2016 Medium

    The KRAB domain was shown to nucleate a protein complex bridging hotspot DNA to the chromosome axis, identifying CXXC1, EWSR1, EHMT2, CDYL, REC8, and synaptonemal proteins as associated factors.

    Evidence Yeast two-hybrid, in vitro binding, and co-immunoprecipitation from spermatocytes

    PMID:27932493

    Open questions at the time
    • Direct versus indirect nature of axis-protein associations not fully resolved
    • Single lab
  15. 2016 High

    A methyltransferase-dead mutant showed that catalytic activity is required for both histone marks and DSB formation, establishing that methylation designates a pool of sites from which breaks are selected.

    Evidence Catalytic-dead PRDM9 mice with ChIP-seq and SSDS DSB mapping, plus dual-variant mice

    PMID:29478809

    Open questions at the time
    • Selection rule determining which marked sites become DSBs not defined
  16. 2017 Medium

    Biophysical characterization revealed an exceptionally stable PRDM9–DNA complex and that only one zinc finger array within the oligomer binds DNA.

    Evidence Gel shift and switchSENSE kinetic/affinity measurements across alleles and DNA variants

    PMID:28155083

    Open questions at the time
    • Exact oligomeric stoichiometry not yet determined
  17. 2017 Medium

    Mapping zinc-finger-mediated multimerization showed that diverged alleles preferentially homo-multimerize, providing a basis for allelic interactions.

    Evidence Co-immunoprecipitation in transfected cells with genome-wide binding/modification mapping

    PMID:29072575

    Open questions at the time
    • Functional consequence of homo- versus hetero-multimers in vivo untested
  18. 2017 Medium

    Demonstrating that the KRAB domain is required for meiosis and that CXXC1 links PRDM9 to the DSB factor IHO1 connected hotspot designation to break initiation machinery.

    Evidence KRAB-truncation mouse with meiotic phenotyping and yeast two-hybrid interaction screens

    PMID:28527011

    Open questions at the time
    • Direct demonstration of the CXXC1–IHO1 bridge in vivo lacking
  19. 2017 Medium

    In vivo PRDM9 ChIP-seq revealed canonical hotspot binding plus noncanonical recruitment to promoters and CTCF sites, indicating axis-associated chromosomal interactions of bound PRDM9.

    Evidence PRDM9 ChIP-seq in spermatocytes with Spo11-null and catalytic-dead controls

    PMID:28336543

    Open questions at the time
    • Biological significance of noncanonical binding unresolved
  20. 2017 Medium

    Identifying intramolecular automethylation of post-SET lysines via the catalytic mechanism revealed an autoregulatory modification of PRDM9.

    Evidence In vitro methyltransferase assays with C321P mutagenesis and mass spectrometry site mapping

    PMID:28126738

    Open questions at the time
    • Functional role of automethylation in vivo unknown
  21. 2019 Medium

    Defining the PRDM9 trimer stoichiometry resolved the oligomeric architecture, showing one DNA-contacting array maintained by two zinc-finger interaction interfaces.

    Evidence EMSA, mass spectrometry, and fluorescence correlation spectroscopy on tagged variants

    PMID:31308055

    Open questions at the time
    • Structural model of the full trimer absent
    • Role of trimer in axis tethering untested
  22. 2019 Medium

    Establishing PRDM9 interaction with cohesins STAG3 and REC8 and a methyltransferase-dependent genetic interaction promoting DSBs linked hotspot marking to axis-localized break formation.

    Evidence Co-IP, Prdm9 × Stag3 genetic epistasis, and DSB focus quantification

    PMID:30853435

    Open questions at the time
    • Direct physical bridge from PRDM9 to axis cohesins not structurally defined
  23. 2019 High

    Characterizing the substrate-competitive inhibitor MRK-740 provided a selective chemical probe that inhibits PRDM9 H3K4 methylation at endogenous loci.

    Evidence Biochemical IC50, inhibitor-enzyme crystal structure, and cell-based ChIP

    PMID:31848333

    Open questions at the time
    • In vivo meiotic application not tested in this study
  24. 2020 High

    Identifying HELLS as the PRDM9 pioneer-complex partner explained how PRDM9 gains chromatin access; loss of HELLS retargets DSBs and causes sterility.

    Evidence Proteomics, conditional Hells knockout, ATAC-seq, ChIP-seq, and DSB mapping

    PMID:32001511 PMID:33047671

    Open questions at the time
    • Order of HELLS recruitment relative to PRDM9 binding incompletely resolved
  25. 2020 High

    Identifying ZCWPW1 as the reader of the combined H3K4me3/H3K36me3 mark assigned the histone signature a function: ZCWPW1 is required for DSB repair and synapsis but not break positioning.

    Evidence Zcwpw1 reader-dead knock-in and knockout mice with ChIP-seq and DMC1 cytology, replicated by two groups

    PMID:32374261 PMID:32744506

    Open questions at the time
    • Molecular steps by which ZCWPW1 promotes repair not fully defined
  26. 2020 Medium

    Demonstrating that PRDM9 asymmetrically traps SPO11 cleavage complexes (SPO11-RI) revealed a role in handling the recombination intermediate downstream of break formation.

    Evidence END-seq detecting SPO11-bound intermediates with Atm-null and Prdm9-null controls

    PMID:32051414

    Open questions at the time
    • Mechanism by which PRDM9 blocks MRE11 not structurally defined
    • Single lab
  27. 2021 Medium

    Showing that CHK2 checkpoint inactivation restores female fertility in Prdm9-null mice revealed a PRDM9-independent recombination route gated by the DNA damage checkpoint.

    Evidence Prdm9-null × Chk2-null double mutant fertility and cytological analysis

    PMID:33097538

    Open questions at the time
    • Nature of the PRDM9-independent recombination system undefined
  28. 2021 Medium

    Linking impaired-activity PRDM9 variants to premature ovarian insufficiency established a human disease connection requiring dosage-dependent methyltransferase activity.

    Evidence Exome sequencing and in vitro methyltransferase assays on patient variants

    PMID:34257419

    Open questions at the time
    • In vitro readout only; in vivo causation not modeled
  29. 2023 Medium

    Identifying CTNNBL1 as a nonhistone substrate broadened PRDM9 enzymatic scope beyond histones.

    Evidence Lysine-oriented peptide library, peptide arrays, in vitro KMT assays, and cell-based methylation validation

    PMID:36972790

    Open questions at the time
    • Biological consequence of CTNNBL1 methylation unknown
  30. 2023 Medium

    Demonstrating PRDM9 induction and H3K4me3-dependent gene activation in brown adipocyte differentiation revealed a non-meiotic somatic function.

    Evidence shRNA and MRK-740 inhibition, ChIP for H3K4me3, and gene expression analysis during adipocyte differentiation

    PMID:37579296

    Open questions at the time
    • Physiological relevance in vivo not established
    • Target gene loci not defined by sequence motif
  31. 2023 Medium

    Establishing FUS/TLS as a PRDM9 partner that also binds REC114 and SPO11 provided a candidate bridge from hotspot complex to break machinery on the axis.

    Evidence Co-IP in vitro and in vivo, immunofluorescence colocalization on axes, and ChIP at H3K4me3 hotspots

    PMID:36967403

    Open questions at the time
    • Functional requirement of FUS/TLS for hotspot-axis tethering not genetically tested
  32. 2025 High

    Showing conserved PRDM9-directed hotspot positioning and motif-erosion-driven turnover in salmonid fish established the deep vertebrate conservation of the mechanism.

    Evidence SSDS/DSB-seq, population recombination maps, genotype-specific comparisons, and ChIP-seq in multiple salmonid species

    PMID:39761307

    Open questions at the time
    • Conservation of the downstream protein complex not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How symmetric PRDM9 binding mechanistically promotes synapsis and repair, and how the full axis-tethering complex assembles in vivo, remain unresolved.
  • No structural model of the PRDM9 trimer engaging axis cohesins
  • Selection rule converting marked sites to actual DSBs undefined
  • Mechanistic basis of binding-symmetry requirement for fertility unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 6 GO:0016740 transferase activity 6 GO:0042393 histone binding 2 GO:0140110 transcription regulator activity 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 1
Pathway
R-HSA-1474165 Reproduction 3 R-HSA-4839726 Chromatin organization 3 R-HSA-1640170 Cell Cycle 2 R-HSA-73894 DNA Repair 2
Partners
CDYLCXXC1EWSR1FUSHELLSREC8STAG3ZCWPW1
Complex memberships
PRDM9 trimerPRDM9–HELLS pioneer complex

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 PRDM9 zinc finger array binds specific DNA sequence motifs at meiotic recombination hotspots, and in vitro binding studies confirmed that the human consensus PRDM9 allele recognizes the 13-mer motif enriched at human hotspots, establishing PRDM9 as the molecular determinant of hotspot positioning. In vitro DNA binding assay; genetic association of PRDM9 zinc finger variants with genome-wide hotspot usage; two mouse strains differing in hotspot usage are polymorphic for the PRDM9 zinc finger array Science High 20044538 20044539 20044541
2009 PRDM9 (Meisetz) possesses histone H3 lysine 4 trimethylase (H3K4me3) activity and is expressed specifically in early meiosis; its deficiency causes sterility in both sexes in mice, establishing it as an essential meiotic histone methyltransferase. Genetic knockout (Prdm9-deficient mice); expression analysis in early meiosis; enzymatic characterization of H3K4me3 activity Science High 20044538 20044539 20044541
2011 Transgenic mice expressing PRDM9 variants with modified zinc fingers show changed hotspot activity, altered H3K4me3 levels at hotspots, and chromosome-wide redistribution of crossovers. PRDM9 variant associated with hotspot activity binds specifically to DNA sequences at hotspot centers in vitro, and cis mutations at hotspot centers that reduce activity also reduce PRDM9 binding, directly demonstrating that PRDM9 DNA-binding specificity determines H3K4me3 deposition and hotspot localization. Transgenic mouse models with modified PRDM9 zinc fingers; in vitro DNA binding assay; ChIP for H3K4me3; genetic crossover mapping PLoS biology High 22028627
2013 Crystal structure of the PRDM9 methyltransferase (PR/SET) domain in complex with histone H3 peptide dimethylated on K4 and S-adenosylhomocysteine revealed the substrate-binding mechanism. PRDM9 catalyzes mono-, di-, and trimethylation of H3K4. Pre-SET and post-SET domains mediate autoinhibition by rearranging substrate and cofactor binding sites. X-ray crystallography (crystal structures of active and autoinhibited states); in vitro methyltransferase activity assays with histone H3 peptide substrates Cell reports High 24095733
2014 The isolated PR/SET domain of PRDM9 trimethylates H3K36 in vitro, and full-length PRDM9 overexpressed in HEK293 cells also significantly increases H3K4me3 and H3K36me3, identifying H3K36 as a second histone substrate of PRDM9. In vitro kinetic methyltransferase assays with histone substrates; overexpression in HEK293 cells with western blot quantification of histone marks Journal of Biological Chemistry High 24634223
2014 PRDM9 binding at hotspots actively reorganizes nucleosomes into a symmetrical pattern, creating an extended nucleosome-depleted region centered on the PRDM9 binding motif. DSBs are centered over this binding motif within the nucleosome-depleted region. H3K4me3-marked regions define the boundaries within which Holliday junction branch migration is restricted. Genome-wide ChIP-seq for histone modifications; MNase-seq for nucleosome positioning; in vitro binding confirmation; genetic cross analysis for crossover boundaries; two inbred mouse strains differing only in PRDM9 zinc finger domain Genome research High 24604780
2016 Full-length PRDM9 trimethylates both H3K4 and H3K36 in vivo in mouse spermatocytes at recombination hotspots. H3K4me3 and H3K36me3 are highly correlated at hotspots but mutually exclusive elsewhere. PRDM9 can place both marks on the same nucleosomes; the K4me3/K36me3 ratio is higher for nucleosomes adjacent to the PRDM9 binding site. Double-positive nucleosomes are dramatically reduced in PRDM9-null mice, confirming PRDM9 dependence. ChIP-seq for H3K4me3 and H3K36me3 in spermatocytes from wild-type and Prdm9-null mice; in vitro methyltransferase assays on same histone molecules; co-detection of dual marks on single nucleosomes PLoS genetics High 27362481
2016 PRDM9 methyltransferase activity is required for H3K4me3 and H3K36me3 deposition and for DSB formation at PRDM9-binding sites. Each PRDM9 variant independently generates its own set of H3K4me3 marks, revealing that PRDM9 binding and subsequent histone methylation designate DSB sites from which a subset is selected for actual DSB formation. Mice expressing methyltransferase-dead PRDM9 (active-site mutation); ChIP-seq for H3K4me3 and H3K36me3; DSB mapping (SSDS); mice carrying two PRDM9 variants with distinct DNA-binding specificities Molecular cell High 29478809
2016 The KRAB domain of PRDM9 interacts directly with CXXC1, EWSR1, EHMT2, and CDYL. PRDM9-bound hotspot complexes also associate with the meiotic cohesin REC8 and synaptonemal complex proteins SYCP3 and SYCP1, suggesting PRDM9 links hotspot DNA to the chromosomal axis. Yeast two-hybrid; in vitro binding assays; co-immunoprecipitation from mouse spermatocytes Molecular biology of the cell Medium 27932493
2017 The KRAB domain of PRDM9 is required for meiosis in mice: truncation of the KRAB domain causes loss of PRDM9 function, altered meiotic prophase, and gametogenesis failure. CXXC1 (a COMPASS complex member) interacts with the KRAB domain and also interacts with IHO1, an essential DSB machinery component, providing a link between hotspot designation and DSB initiation. KRAB domain truncation mouse model (in vivo); yeast two-hybrid screens for KRAB domain interactors; phenotypic analysis of meiotic prophase Chromosoma Medium 28527011
2015 PRDM9 nuclear localization is restricted to pre-leptonema to early leptonema in male germ cells and is no longer detectable by late zygonema. PRDM9-dependent H3K4me3 marks disappear by pachytene. PRDM9 is not required for incorporation of cohesin complexes into chromosomal axial elements. In the absence of PRDM9, homology recognition and synapsis are inefficient with aberrant DSB repair. Immunofluorescence with spermatogenic stage-specific markers; comparison of wild-type versus Prdm9-null germ cells; quantification of RAD51 foci Chromosoma Medium 25894966
2017 In vivo ChIP-seq of PRDM9 in mouse spermatocytes identified canonical hotspot binding but also revealed noncanonical recruitment to gene promoters (DSB-dependent) and to CTCF binding sites (DSB-independent), suggesting that hotspot-bound PRDM9 interacts with genomic sequences on the chromosome axis. ChIP-seq for PRDM9 in mouse spermatocytes; comparison with Spo11-null and PRDM9 methyltransferase-dead backgrounds Genome research Medium 28336543
2017 PRDM9 zinc fingers also mediate multimerization in addition to DNA binding. Highly diverged alleles of PRDM9 preferentially form homo-multimers rather than hetero-multimers. Co-immunoprecipitation in transfected human cell line; mapping of PRDM9 binding and histone modifications genome-wide eLife Medium 29072575
2015 PRDM9 forms functional heteromeric complexes in cell culture; in heterozygous mice, the stronger PRDM9 allele suppresses chromatin modification and recombination at hotspots of the weaker allele (allelic competition/suppression). PRDM9 function is dosage sensitive: Prdm9+/- mice have reduced numbers and less active hotspots. Cell culture co-expression of PRDM9 protein variants; ChIP-seq for H3K4me3 in heterozygous and hemizygous mouse models; genetic crossover analysis PLoS genetics Medium 26368021
2016 Humanizing the DNA-binding zinc finger domain of PRDM9 in C57BL/6 mice repositions DSB hotspots and completely restores fertility in male hybrids. The degree to which a PRDM9 variant binds both homologues symmetrically at DSB sites (symmetric PRDM9 binding) strongly correlates with fertility measures, indicating that binding symmetry plays a downstream role in the recombination process. Knock-in mouse model (humanized PRDM9 DNA-binding domain); ChIP-seq for PRDM9 binding and DSB mapping (SSDS); hybrid fertility assays Nature High 26840484
2016 Crystal structure of PRDM9 allele A zinc fingers 8–11 co-crystallized with a hotspot oligonucleotide revealed that each α-helix contacts up to four adjacent DNA bases in the major groove, with conserved His or Arg residues contacting C:G base pairs and Asn contacting T:A. Allele C binds its cognate hotspot with higher affinity than allele A, explaining allele C dominance in heterozygotes. X-ray co-crystallography (ZnF8-12 of hPRDM9A with hotspot DNA); in vitro binding affinity measurements for multiple alleles Genes & development High 26833727
2017 Crystal structure of PRDM9 allele C zinc fingers 8–13 co-crystallized with a PRDM9c-specific hotspot sequence showed three structural differences from allele A: Ser764 in ZF9 accommodates variable bases (vs. Arg764 recognizing conserved G in allele A); a two-finger expansion in ZF11 recognizes three additional base pairs; an Arg-Asp dipeptide switch allows identical ZF modules to recognize different sequences. X-ray co-crystallography (ZnF8-13 of hPRDM9C with cognate hotspot DNA); structural comparison with PRDM9A complex Journal of Biological Chemistry High 28801461
2020 HELLS (a SNF2-like chromatin remodeler) is recruited to recombination hotspots by PRDM9 and is necessary for PRDM9 binding, histone modifications (H3K4me3, H3K36me3), and DNA accessibility at hotspots. In male mice lacking HELLS, DSBs are retargeted to other open chromatin sites, causing germ cell death and sterility. HELLS and PRDM9 form a pioneer complex to create open chromatin at hotspots. Proteomic identification of PRDM9 partners; conditional Hells knockout mice; ATAC-seq for chromatin accessibility; ChIP-seq for histone marks and PRDM9 binding; DSB mapping Genes & development High 32001511
2020 PRDM9 activity (binding and histone modification) depends on HELLS for chromatin access at PRDM9-directed hotspots. HELLS is also essential for 5-hydroxymethylcytosine (5hmC) enrichment at PRDM9 sites. 5hmC is triggered by PRDM9 binding and histone modification independently of DSB formation. Proteomic approaches for PRDM9 partner identification; conditional Hells knockout mouse; ChIP-seq; 5hmC mapping in Spo11-null and PRDM9 methyltransferase-dead mice eLife High 33047671
2020 PRDM9 asymmetrically blocks MRE11 from releasing SPO11 after DSB formation, creating a SPO11-bound meiotic recombination intermediate (SPO11-RI) at all hotspots. ATM kinase is required for MRE11-initiated resection to release trapped SPO11 cleavage complexes. END-seq on mouse spermatocytes with enzymatic modifications to detect SPO11-bound intermediates; Atm-/- spermatocyte analysis; PRDM9-null comparisons Nature communications Medium 32051414
2019 PRDM9 interacts with the meiotic cohesin subunit STAG3 and REC8. These interactions promote normal levels of meiotic DSBs at recombination hotspots in spermatocytes. The efficacy of the Prdm9-Stag3 genetic interaction in promoting DSB formation depends on PRDM9 methyltransferase activity. STAG3 and REC8 promote axis localization of DSB-promoting proteins HORMAD1, IHO1, MEI4, and SPO11 activity. Co-immunoprecipitation for protein interactions; genetic interaction analysis (Prdm9 × Stag3 double mutants); immunofluorescence quantification of DSB foci Current Biology Medium 30853435
2020 ZCWPW1 is recruited to recombination hotspots by PRDM9 in a largely PRDM9-dependent manner and recognizes the combination of H3K4me3 and H3K36me3 deposited by PRDM9. Zcwpw1 knockout mice show completely normal DSB positioning but persistent DMC1 foci, severe DSB repair and synapsis defects, and sterility, establishing ZCWPW1 as the reader of PRDM9-deposited histone marks required for DSB repair. H3K4me3 reader-dead Zcwpw1 knock-in mice; Zcwpw1 knockout mice; ChIP-seq in multiple mutant backgrounds; immunofluorescence for DMC1 foci eLife High 32374261 32744506
2018 Deletion of the KRAB domain in mice results in only residual PRDM9 methyltransferase activity in vivo and meiotic arrest, although the KRAB domain is not essential for methyltransferase activity in cell culture. Neither the KRAB, SSXRD, nor post-SET zinc finger domains of PRDM9 regulate meiotic gene expression. KRAB domain deletion mouse model; cell culture methyltransferase activity assays; germline transcriptome analysis (mRNA and miRNA) comparing Prdm9 KRAB-deleted and wild-type males Genetics Medium 29674518
2019 MRK-740 is a potent (IC50 ~80 nM) PRDM9 inhibitor that binds in the substrate-binding pocket with extensive interactions with the SAM cofactor, conferring SAM-dependent substrate-competitive inhibition. In cells, MRK-740 specifically inhibits H3K4 methylation at endogenous PRDM9 target loci. Biochemical inhibition assay; crystal structure of inhibitor-enzyme complex; cell-based ChIP assay for H3K4me3 at PRDM9 target loci Nature communications High 31848333
2017 The PRDM9 zinc finger array forms a highly stable complex with its DNA recognition sequence with a dissociation half-time of many hours and nanomolar KD. Polymorphisms in the recognition sequence directly affect binding affinity. Only one ZnF array within the PRDM9 oligomer binds DNA, and longer binding targets are preferred than predicted from the number of ZnFs. Gel mobility shift assays; switchSENSE biophysical measurements of binding kinetics and affinity; analysis of multiple PRDM9 alleles and DNA variants Chromosome research Medium 28155083
2019 PRDM9 forms a trimer: the ZnF array alone is sufficient for multimerization, at least five ZnFs are required for trimer formation, and the stoichiometry is maintained in the free soluble protein. Only one ZnF array within the PRDM9 trimer contacts DNA; the remaining two ZnF arrays maintain the trimer through ZnF-ZnF interactions. Electrophoretic mobility shift assays; mass spectrometry; fluorescence correlation spectroscopy; analysis of tagged protein variants from different expression systems Life science alliance Medium 31308055
2017 PRDM9 performs intramolecular automethylation on multiple lysine residues in a lysine-rich region of the post-SET domain. Automethylation is abolished by the active-site mutation C321P (which also disrupts SAM interaction), establishing that automethylation uses the same catalytic mechanism as histone methylation. In vitro methyltransferase assays; active-site mutagenesis (C321P); mass spectrometry to identify automethylation sites; rational design of peptidic inhibitor Biochemical Journal Medium 28126738
2014 PRDM9 requires the full array of 11 or 12 contiguous zinc fingers for hotspot DNA binding, and in vitro binding parallels in vivo biological activity. Individual nucleotide positions along the binding site vary considerably in tolerance of substitutions, and the protein makes additional contacts to the DNA phosphate backbone. In vitro electrophoretic mobility shift assay with systematic mutagenesis of hotspot binding sites; comparison of four hotspot sequences with two PRDM9 alleles Genome biology Medium 23618393
2014 A single C321P mutation in the PR/SET domain of PRDM9 significantly weakens its methyltransferase activity. Characterization of PRDM9-methylated recombinant histone octamers identified new histone substrates for the enzyme. Site-directed mutagenesis (C321P); biochemical methyltransferase assays with recombinant histone octamers and peptides; biophysical characterization Biochemical Journal Medium 24785241
2020 EWSR1 binds both PRDM9 and phosphorylated REC8 (pREC8) in male meiotic cells. Conditional knockout of Ewsr1 before meiosis onset causes meiotic arrest with decreased histone trimethylation at hotspots, impaired DSB repair, and reduced crossover number, demonstrating EWSR1 is essential for promoting PRDM9-dependent histone methylation and linking hotspots to the chromosome axis. Co-immunoprecipitation from meiotic cells; conditional Ewsr1 knockout mouse; ChIP for H3K4me3/H3K36me3 at hotspots; immunofluorescence for DSB repair markers Molecular biology of the cell Medium 33175657
2023 PRDM9 methylates nonhistone protein CTNNBL1 in cells, as identified by lysine-oriented peptide library screening, peptide spot arrays, in vitro KMT reactions on recombinant proteins, and cell-based validation. PRDM9 preferentially methylates peptide sequences not found in histone proteins. Lysine-oriented peptide library screening; peptide spot arrays; in vitro KMT assays on recombinant proteins; cell-based methylation assays; multisite λ-dynamics computational analysis Journal of Biological Chemistry Medium 36972790
2023 In mouse brown adipocytes, PRDM9 is robustly induced during differentiation downstream of glutamine/C/EBPβ signaling, and its inactivation (shRNA or inhibitor) attenuates glutamine-triggered H3K4me3-mediated transcriptional induction of adipogenic and thermogenic gene programs, demonstrating a non-meiotic role for PRDM9 in somatic cell differentiation. shRNA knockdown; pharmacological inhibition (MRK-740); ChIP for H3K4me3; gene expression analysis in brown adipocyte differentiation; C/EBPβ ChIP at Prdm9 enhancer Diabetes Medium 37579296
2023 FUS/TLS physically interacts with PRDM9 and colocalizes with it on meiotic chromosome axes. FUS/TLS also interacts with REC114 (an axis-bound SPO11 auxiliary factor) and co-immunoprecipitates with SPO11 in vitro and in vivo, suggesting FUS/TLS links the PRDM9-hotspot complex to the DSB initiation machinery. ChIP shows FUS/TLS localizes at H3K4me3-marked hotspots. Co-immunoprecipitation in vitro and in vivo; immunofluorescence with synaptonemal complex marker SYCP3; ChIP at H3K4me3 hotspots Cellular and Molecular Life Sciences Medium 36967403
2021 In mice lacking PRDM9, the meiotic DNA damage checkpoint protein CHK2 acts as a sex-specific modifier: CHK2 inactivation allows female-specific fertility in the absence of PRDM9, revealing that a PRDM9-independent recombination system is compatible with female meiosis when the checkpoint is bypassed. Prdm9-null × Chk2-null double mutant mouse models; fertility assays; cytological analysis of meiosis in female and male mice Science advances Medium 33097538
2025 In salmonid fish (Oncorhynchus mykiss), full-length PRDM9 drives DSB hotspot positioning away from promoters and toward intergenic sites enriched for H3K4me3 and H3K36me3. Hotspot positions depend on Prdm9 genotype, and rapid hotspot turnover is caused by PRDM9 target motif erosion, demonstrating that PRDM9 function in directing recombination is conserved across vertebrates. Genome-wide DSB mapping (SSDS/DSB-seq) in rainbow trout testes; population-scaled recombination maps in multiple salmonid species; Prdm9 genotype-specific hotspot comparisons; ChIP-seq for H3K4me3 and H3K36me3 PLoS biology High 39761307
2021 Functional variants in PRDM9 identified in patients with premature ovarian insufficiency impair its methyltransferase activity in vitro, establishing dosage-dependent PRDM9 methyltransferase activity as required for ovarian function in humans. Exome sequencing; in vitro methyltransferase activity assays on patient-derived PRDM9 variants Genetics in Medicine Medium 34257419

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 PRDM9 is a major determinant of meiotic recombination hotspots in humans and mice. Science (New York, N.Y.) 773 20044539
2009 Drive against hotspot motifs in primates implicates the PRDM9 gene in meiotic recombination. Science (New York, N.Y.) 521 20044541
2009 Prdm9 controls activation of mammalian recombination hotspots. Science (New York, N.Y.) 459 20044538
2009 Accelerated evolution of the Prdm9 speciation gene across diverse metazoan taxa. PLoS genetics 230 19997497
2016 Re-engineering the zinc fingers of PRDM9 reverses hybrid sterility in mice. Nature 154 26840484
2016 The Meiotic Recombination Activator PRDM9 Trimethylates Both H3K36 and H3K4 at Recombination Hotspots In Vivo. PLoS genetics 137 27362481
2011 Mouse PRDM9 DNA-binding specificity determines sites of histone H3 lysine 4 trimethylation for initiation of meiotic recombination. PLoS biology 136 22028627
2018 PRDM9 and Its Role in Genetic Recombination. Trends in genetics : TIG 112 29366606
2011 Death of PRDM9 coincides with stabilization of the recombination landscape in the dog genome. Genome research 110 22006216
2011 Variants of the protein PRDM9 differentially regulate a set of human meiotic recombination hotspots highly active in African populations. Proceedings of the National Academy of Sciences of the United States of America 108 21750151
2015 PRDM9 drives evolutionary erosion of hotspots in Mus musculus through haplotype-specific initiation of meiotic recombination. PLoS genetics 106 25568937
2014 PRDM9 binding organizes hotspot nucleosomes and limits Holliday junction migration. Genome research 106 24604780
2020 ATM and PRDM9 regulate SPO11-bound recombination intermediates during meiosis. Nature communications 96 32051414
2014 Trimethylation of histone H3 lysine 36 by human methyltransferase PRDM9 protein. The Journal of biological chemistry 95 24634223
2018 PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites. Molecular cell 94 29478809
2013 Molecular basis for the regulation of the H3K4 methyltransferase activity of PRDM9. Cell reports 90 24095733
2018 PRDM9, a driver of the genetic map. PLoS genetics 85 30161134
2017 A map of human PRDM9 binding provides evidence for novel behaviors of PRDM9 and other zinc-finger proteins in meiosis. eLife 81 29072575
2016 PRDM9 interactions with other proteins provide a link between recombination hotspots and the chromosomal axis in meiosis. Molecular biology of the cell 76 27932493
2017 The PRDM9 KRAB domain is required for meiosis and involved in protein interactions. Chromosoma 66 28527011
2011 What are the genomic drivers of the rapid evolution of PRDM9? Trends in genetics : TIG 66 21388701
2009 Extraordinary molecular evolution in the PRDM9 fertility gene. PloS one 66 20041164
2013 DNA binding specificities of the long zinc-finger recombination protein PRDM9. Genome biology 64 23618393
2014 Primate evolution of the recombination regulator PRDM9. Nature communications 62 25001002
2015 Affinity-seq detects genome-wide PRDM9 binding sites and reveals the impact of prior chromatin modifications on mammalian recombination hotspot usage. Epigenetics & chromatin 61 26351520
2011 The case of the fickle fingers: how the PRDM9 zinc finger protein specifies meiotic recombination hotspots in humans. PLoS biology 61 22162947
2012 Interallelic and intergenic incompatibilities of the Prdm9 (Hst1) gene in mouse hybrid sterility. PLoS genetics 58 23133405
2014 Diversity of Prdm9 zinc finger array in wild mice unravels new facets of the evolutionary turnover of this coding minisatellite. PloS one 57 24454780
2020 HELLS and PRDM9 form a pioneer complex to open chromatin at meiotic recombination hot spots. Genes & development 53 32001511
2017 In vivo binding of PRDM9 reveals interactions with noncanonical genomic sites. Genome research 53 28336543
2011 Prdm9, a major determinant of meiotic recombination hotspots, is not functional in dogs and their wild relatives, wolves and coyotes. PloS one 53 22102853
2015 Nuclear localization of PRDM9 and its role in meiotic chromatin modifications and homologous synapsis. Chromosoma 52 25894966
2014 Prdm9 polymorphism unveils mouse evolutionary tracks. DNA research : an international journal for rapid publication of reports on genes and genomes 50 24449848
2016 Structural basis for human PRDM9 action at recombination hot spots. Genes & development 48 26833727
2018 Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice. eLife 47 29537370
2020 Snake Recombination Landscapes Are Concentrated in Functional Regions despite PRDM9. Molecular biology and evolution 43 31926008
2020 The histone modification reader ZCWPW1 links histone methylation to PRDM9-induced double-strand break repair. eLife 43 32374261
2015 Multimer Formation Explains Allelic Suppression of PRDM9 Recombination Hotspots. PLoS genetics 42 26368021
2014 Genetic recombination variation in wild Robertsonian mice: on the role of chromosomal fusions and Prdm9 allelic background. Proceedings. Biological sciences 42 24850922
2012 Rare allelic forms of PRDM9 associated with childhood leukemogenesis. Genome research 41 23222848
2012 Recombination regulator PRDM9 influences the instability of its own coding sequence in humans. Proceedings of the National Academy of Sciences of the United States of America 41 23267059
2009 Single-nucleotide polymorphisms of the PRDM9 (MEISETZ) gene in patients with nonobstructive azoospermia. Journal of andrology 39 19168450
2020 ZCWPW1 is recruited to recombination hotspots by PRDM9 and is essential for meiotic double strand break repair. eLife 38 32744506
2006 Meisetz, a novel histone tri-methyltransferase, regulates meiosis-specific epigenesis. Cell cycle (Georgetown, Tex.) 37 16582607
2021 Hybrid sterility genes in mice (Mus musculus): a peculiar case of PRDM9 incompatibility. Trends in genetics : TIG 34 34238593
2018 Aberrant PRDM9 expression impacts the pan-cancer genomic landscape. Genome research 34 30341163
2014 Prdm9 incompatibility controls oligospermia and delayed fertility but no selfish transmission in mouse intersubspecific hybrids. PloS one 34 24756080
2022 PRDM9 losses in vertebrates are coupled to those of paralogs ZCWPW1 and ZCWPW2. Proceedings of the National Academy of Sciences of the United States of America 33 35217607
2019 Histone methyltransferase PRDM9 is not essential for meiosis in male mice. Genome research 33 31186301
2019 Discovery of a chemical probe for PRDM9. Nature communications 32 31848333
2019 Prdm9 and Meiotic Cohesin Proteins Cooperatively Promote DNA Double-Strand Break Formation in Mammalian Spermatocytes. Current biology : CB 31 30853435
2012 High diversity at PRDM9 in chimpanzees and bonobos. PloS one 30 22768294
2008 Two single nucleotide polymorphisms in PRDM9 (MEISETZ) gene may be a genetic risk factor for Japanese patients with azoospermia by meiotic arrest. Journal of assisted reproduction and genetics 30 18941885
2024 Patterns of recombination in snakes reveal a tug-of-war between PRDM9 and promoter-like features. Science (New York, N.Y.) 29 38386752
2014 Characterization of the histone methyltransferase PRDM9 using biochemical, biophysical and chemical biology techniques. The Biochemical journal 28 24785241
2013 Characterization of Prdm9 in equids and sterility in mules. PloS one 26 23613924
2021 Rat PRDM9 shapes recombination landscapes, duration of meiosis, gametogenesis, and age of fertility. BMC biology 24 33910563
2021 Pathogenic variants of meiotic double strand break (DSB) formation genes PRDM9 and ANKRD31 in premature ovarian insufficiency. Genetics in medicine : official journal of the American College of Medical Genetics 24 34257419
2021 Cataloging Human PRDM9 Allelic Variation Using Long-Read Sequencing Reveals PRDM9 Population Specificity and Two Distinct Groupings of Related Alleles. Frontiers in cell and developmental biology 24 34805134
2020 PRDM9 activity depends on HELLS and promotes local 5-hydroxymethylcytosine enrichment. eLife 24 33047671
2020 Prdm9 Intersubspecific Interactions in Hybrid Male Sterility of House Mouse. Molecular biology and evolution 23 32642764
2019 Genomic Structure of Hstx2 Modifier of Prdm9-Dependent Hybrid Male Sterility in Mice. Genetics 21 31562180
2023 Glutamine Production by Glul Promotes Thermogenic Adipocyte Differentiation Through Prdm9-Mediated H3K4me3 and Transcriptional Reprogramming. Diabetes 20 37579296
2024 High prevalence of PRDM9-independent recombination hotspots in placental mammals. Proceedings of the National Academy of Sciences of the United States of America 19 38809707
2018 Interrogating the Functions of PRDM9 Domains in Meiosis. Genetics 19 29674518
2016 Evolutionary dynamics of meiotic recombination hotspots regulator PRDM9 in bovids. Molecular genetics and genomics : MGG 18 27744561
2019 PRDM9 Diversity at Fine Geographical Scale Reveals Contrasting Evolutionary Patterns and Functional Constraints in Natural Populations of House Mice. Molecular biology and evolution 17 31004162
2017 Structural basis of human PR/SET domain 9 (PRDM9) allele C-specific recognition of its cognate DNA sequence. The Journal of biological chemistry 17 28801461
2020 Sexual dimorphism in the meiotic requirement for PRDM9: A mammalian evolutionary safeguard. Science advances 16 33097538
2020 EWSR1 affects PRDM9-dependent histone 3 methylation and provides a link between recombination hotspots and the chromosome axis protein REC8. Molecular biology of the cell 15 33175657
2018 Construction of PRDM9 allele-specific recombination maps in cattle using large-scale pedigree analysis and genome-wide single sperm genomics. DNA research : an international journal for rapid publication of reports on genes and genomes 15 29186399
2023 Identification of nonhistone substrates of the lysine methyltransferase PRDM9. The Journal of biological chemistry 14 36972790
2018 Cisplatin-induced DNA double-strand breaks promote meiotic chromosome synapsis in PRDM9-controlled mouse hybrid sterility. eLife 14 30592461
2017 The long zinc finger domain of PRDM9 forms a highly stable and long-lived complex with its DNA recognition sequence. Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology 14 28155083
2024 Multiple Genomic Landscapes of Recombination and Genomic Divergence in Wild Populations of House Mice-The Role of Chromosomal Fusions and Prdm9. Molecular biology and evolution 13 38513632
2021 Altering the Binding Properties of PRDM9 Partially Restores Fertility across the Species Boundary. Molecular biology and evolution 13 34491357
2019 Depletion of PRDM9 enhances proliferation, migration and chemotaxis potentials in human periodontal ligament stem cells. Connective tissue research 13 31096797
2016 Zinc Finger Domain of the PRDM9 Gene on Chromosome 1 Exhibits High Diversity in Ruminants but Its Paralog PRDM7 Contains Multiple Disruptive Mutations. PloS one 12 27203728
2016 Evidence of positive selection and concerted evolution in the rapidly evolving PRDM9 zinc finger domain in goats and sheep. Animal genetics 12 27621101
2022 The KRAB Domain of ZNF10 Guides the Identification of Specific Amino Acids That Transform the Ancestral KRAB-A-Related Domain Present in Human PRDM9 into a Canonical Modern KRAB-A Domain. International journal of molecular sciences 11 35162997
2017 Discovery and characterisation of the automethylation properties of PRDM9. The Biochemical journal 11 28126738
2012 Evaluation of PRDM9 variation as a risk factor for recurrent genomic disorders and chromosomal non-disjunction. Human genetics 11 22643917
2025 PRDM9 drives the location and rapid evolution of recombination hotspots in salmonid fish. PLoS biology 10 39761307
2024 Bridging the gap between the evolutionary dynamics and the molecular mechanisms of meiosis: A model based exploration of the PRDM9 intra-genomic Red Queen. PLoS genetics 10 38768268
2019 PRDM9 and the evolution of recombination hotspots. Theoretical population biology 10 30660607
2023 Cancer Associated PRDM9: Implications for Linking Genomic Instability and Meiotic Recombination. International journal of molecular sciences 8 38003713
2020 Meiotic epigenetic factor PRDM9 impacts sperm quality of hybrid mice. Reproduction (Cambridge, England) 8 32272448
2018 Prenatal diagnosis of a familial 5p14.3-p14.1 deletion encompassing CDH18, CDH12, PMCHL1, PRDM9 and CDH10 in a fetus with congenital heart disease on prenatal ultrasound. Taiwanese journal of obstetrics & gynecology 8 30342662
2010 PRDM9 sticks its zinc fingers into recombination hotspots and between species. F1000 biology reports 8 20948797
2022 Genic and chromosomal components of Prdm9-driven hybrid male sterility in mice (Mus musculus). Genetics 7 35924978
2016 Variation in the Zinc Finger of PRDM9 is Associated with the Absence of Recombination along Nondisjoined Chromosomes 21 of Maternal Origin. Journal of Down Syndrome & chromosome abnormalities 7 28702511
2019 PRDM9 forms a trimer by interactions within the zinc finger array. Life science alliance 6 31308055
2019 Bos taurus-indicus hybridization correlates with intralocus sexual-conflict effects of PRDM9 on male and female fertility in Holstein cattle. BMC genetics 6 31462216
2016 The pioneering role of PRDM9 indel mutations in tarsier evolution. Scientific reports 6 27698394
2013 The complex binding of PRDM9. Genome biology 6 23651476
2023 The RNA-binding protein FUS/TLS interacts with SPO11 and PRDM9 and localize at meiotic recombination hotspots. Cellular and molecular life sciences : CMLS 5 36967403
2024 Natural variation in the zinc-finger-encoding exon of Prdm9 affects hybrid sterility phenotypes in mice. Genetics 4 38217871
2023 The Recombination Hotspot Paradox: Co-evolution between PRDM9 and its target sites. Theoretical population biology 4 37451508
2022 Evolution of the recombination regulator PRDM9 in minke whales. BMC genomics 4 35296233
2021 PRDM9-directed recombination hotspots depleted near meiotically transcribed genes. Gene 4 34952174

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