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Showing KLC1 — KLC is a alias.

KLC1

Kinesin light chain 1 · UniProt Q07866

Length
573 aa
Mass
65.3 kDa
Annotated
2026-06-10
27 papers in source corpus 16 papers cited in narrative 15 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KLC1 is the cargo-binding light chain subunit of kinesin-1, coupling diverse cargoes to microtubule-based anterograde transport while regulating motor activation (PMID:22404616, PMID:30026235). Its tetratricopeptide repeat (TPR) domain recognizes short linear motifs on cargo adaptors, including the WD motif of Alcadein-α and the W-acidic/JIP1 motif, which bind a shared TPR footprint defined by seven critical residues and partially overlap with the autoinhibitory LFP-acidic motif of KLC1 itself (PMID:22404616, PMID:30026235). Cargo-SLiM engagement is the activating signal: it dislocates the TPR 'shoulder' formed by docking of KHC coiled-coil 1 onto the KLC TPR in the autoinhibited heterotetramer, in which the KLC TPR also wedges between motor domains and its C-terminal helices occlude the cargo-binding interface as a second autoinhibitory layer [PMID:bio_10.1101_2025.07.15.665000, PMID:bio_10.1101_2025.04.08.647705]. This breadth of adaptor recognition lets KLC1 select among physiologically distinct cargoes—SFPQ-RNA granules for long-distance axonal transport (PMID:33284322), APP/JIP1b vesicles (PMID:29093025), RPE phagosomes derived from photoreceptor outer segments (PMID:26261180), and insulin-stimulated GLUT4 vesicles via DOC2B (PMID:30707251)—with several of these interactions gated by phosphorylation: Thr466 phosphorylation, which rises in aged brain, abolishes JIP1b binding and the enhanced fast velocity of APP transport (PMID:29093025), while DOC2B Tyr301 phosphorylation upon insulin stimulation promotes KLC1 binding and GLUT4 surface accumulation (PMID:30707251). Transport output is further tuned at the cargo level, since KLC-bound motors retain partial autoinhibition that shapes directionality at microtubule intersections [PMID:bio_10.1101_2025.05.06.652443], and at the transcript level, where CELF1 binds KLC1 mRNA and represses its splice variant E (PMID:38768546). Loss of KLC1 reduces phagosome run length and impairs degradation, producing age-related macular degeneration-like RPE pathology in mice (PMID:26261180), and disruption of the KLC1-SFPQ interaction by Charcot-Marie-Tooth-associated KIF5A mutations compromises axon survival (PMID:33284322).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1993 Medium

    Establishing the primary structure of human KLC1 was the prerequisite for assigning its modular architecture, revealing N-terminal heptad (rod) repeats and central/C-terminal repeat units that would later be recognized as the cargo-binding and regulatory domains.

    Evidence cDNA cloning, sequencing, heterologous expression in bacteria and CHO cells, chromosomal mapping

    PMID:8274221

    Open questions at the time
    • Did not assign function to any domain
    • No interaction partners or cargo identified
    • Repeat regions not yet linked to TPR cargo recognition
  2. 2012 High

    Defining a minimal 10-residue WD motif in Alcadein-α that activates kinesin-1 through the KLC1 TPR established that short cargo motifs, not just stable docking, drive motor activation and anterograde transport.

    Evidence In vivo transport assays with artificial WD-motif transmembrane proteins, excess-KLC1 competition, TPR domain-deletion analysis

    PMID:22404616

    Open questions at the time
    • Structural basis of how WD binding releases motor autoinhibition not resolved
    • Only part of TPR required, but the activating allosteric step undefined
  3. 2014 Low

    A yeast two-hybrid link between KLC1 and the fission protein Dnm1L/DRP1 raised the possibility that KLC1 mediates post-fission mitochondrial transport independently of direct KIF5 binding.

    Evidence Yeast two-hybrid screen and co-localization in cultured cells

    PMID:25082190

    Open questions at the time
    • Yeast two-hybrid and co-localization only; no co-IP or reciprocal validation
    • No functional mitochondrial transport assay in mammalian cells
    • Single lab, unconfirmed
  4. 2015 High

    Genetic loss of KLC1 separated cargo speed from processivity in vivo, showing KLC1 controls phagosome run length, localization, and degradation rather than velocity, and links this to age-related RPE pathology.

    Evidence Live-cell imaging of RPE phagosomes plus KLC1 knockout mice with AMD-like phenotypic analysis

    PMID:26261180

    Open questions at the time
    • Cargo adaptor coupling phagosomes to KLC1 not identified
    • Molecular basis of run-length dependence on KLC1 unresolved
  5. 2017 High

    Demonstrating that Thr466 phosphorylation selectively abolishes the JIP1b interaction and the fast-velocity mode of APP transport, while sparing a separate coiled-coil-mediated interaction, established phosphorylation as a cargo- and mode-specific regulatory switch relevant to brain aging.

    Evidence Phosphomimetic mutagenesis (T466E), in vivo transport velocity measurement, co-IP, aged brain biochemistry

    PMID:29093025

    Open questions at the time
    • Kinase responsible for Thr466 phosphorylation not identified
    • Direct causal link between Thr466 phosphorylation and aging phenotype not established
  6. 2018 High

    Quantitative mapping of seven TPR residues critical for JIP1 binding, and the demonstration that JIP1 and Alcadein-α compete for the same site overlapping the autoinhibitory LFP-acidic motif, defined the molecular footprint of cargo recognition and intramolecular autoinhibition.

    Evidence Isothermal titration calorimetry with truncated TPR fragments, residue mutagenesis, footprinting against the KLC1-TPR:JIP1 crystal structure

    PMID:30026235

    Open questions at the time
    • Does not show how cargo binding relieves whole-motor autoinhibition
    • Affinity hierarchy among competing cargoes in cells not resolved
  7. 2019 High

    Showing that insulin-stimulated DOC2B Tyr301 phosphorylation drives KLC1 binding and GLUT4 plasma-membrane accumulation extended KLC1's role to signal-dependent metabolic cargo delivery in skeletal muscle.

    Evidence Y301 mutagenesis, co-IP, mass spectrometry, skeletal-muscle transgenic mice, GLUT4 surface assays

    PMID:30707251

    Open questions at the time
    • Whether DOC2B engages the canonical TPR SLiM site not defined
    • Identity of the DOC2B Y301 kinase not established
  8. 2009 Medium

    Testing whether AMPK-mediated KLC1 phosphorylation regulates insulin-granule transport yielded a negative result, constraining the set of functionally relevant phosphosites by showing Ser517/520 modification does not alter granule dynamics.

    Evidence In vitro AMPK kinase assay on GST-KLC1, phosphomutant overexpression in MIN6 cells, 3D live-cell imaging, phospho-specific antibody; replicated in companion paper

    PMID:20074060 PMID:21099273

    Open questions at the time
    • In vitro phosphorylation occurs but no cellular function identified
    • Does not exclude regulation under conditions not tested
  9. 2021 High

    Identifying SFPQ as a KLC1-selected cargo within a KIF5A/KLC1 complex required for long-distance axonal RNA-granule transport, and showing CMT-causing KIF5A mutations disrupt this, established KLC1 as an adaptor for RNA-granule transport with disease relevance.

    Evidence Reciprocal co-IP, CMT-mutant loss-of-function, axon degeneration assays, therapeutic rescue

    PMID:33284322

    Open questions at the time
    • KLC1 SLiM/motif on SFPQ not mapped
    • Whether KLC1 directly contacts SFPQ or via another adaptor not resolved
  10. 2024 Medium

    Defining CELF1 as a direct binder of KLC1 mRNA that represses splice variant E added a transcript-level layer of regulation governing which KLC1 isoform is produced.

    Evidence CELF1 depletion/overexpression, CLIP-seq analysis, human brain transcriptomic correlation

    PMID:38768546

    Open questions at the time
    • Functional consequence of the splice switch on KLC1 transport activity not tested
    • Physiological contexts driving CELF1 control of KLC1 unclear
  11. 2024 Medium

    Mapping a CRMP2 residue (R565/R566) required for KLC1 binding and showing klc1a phenocopies crmp2 knockdown in zebrafish commissure formation extended KLC1 cargo recognition to a neurodevelopmental adaptor.

    Evidence Co-IP of CRMP2 WT vs R566C mutant, zebrafish klc1a morpholino knockdown, crmp2 knockdown comparison

    PMID:38830696

    Open questions at the time
    • Single lab, zebrafish model only
    • Mammalian validation of the CRMP2-KLC1 interaction lacking
  12. 2025 High

    Cryo-EM of the autoinhibited heterotetramer resolved the structural logic of KLC autoinhibition—TPR domains wedge between motor domains and KLC C-terminal helices occlude the cargo-binding interface—providing the framework for how cargo and regulators release the motor.

    Evidence Cryo-EM structure, crosslinking mass spectrometry, functional motility studies (preprint)

    PMID:bio_10.1101_2025.07.15.665000

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Dynamics of the autoinhibition-to-active transition inferred, not directly captured
  13. 2025 Medium

    Showing that cargo-adaptor SLiM binding dislocates the TPR shoulder formed by KHC coiled-coil 1 and facilitates MAP7 recruitment provided a direct allosteric mechanism linking cargo recognition to motor activation.

    Evidence Protein design, computational modelling, EM of the holoenzyme with and without SLiM peptides (preprint)

    PMID:bio_10.1101_2025.04.08.647705

    Open questions at the time
    • Preprint, single lab
    • Kinetics of the shoulder dislocation step not quantified
  14. 2025 Medium

    Reconstituted liposome transport showed KLC retains partial autoinhibition even when cargo-bound, reducing run length and landing rate and tuning directionality, reframing KLC as a continuous regulator rather than a simple on/off switch.

    Evidence In vitro liposome and single-MT motility assays, kinesore pharmacological rescue, in silico modeling (preprint)

    PMID:bio_10.1101_2025.05.06.652443

    Open questions at the time
    • Preprint, single lab
    • Generality of residual autoinhibition across different cargoes not established
  15. 2025 Medium

    Identifying KLC1 as a host factor co-opted by dengue virus NS1 for replication and lipid droplet organization in mosquito cells extended KLC1's transport function to viral pathogenesis.

    Evidence Proximity ligation, reciprocal co-IP, immunoelectron microscopy, siRNA silencing, peptide competition, viral titer/genome quantification (preprint)

    PMID:40166163

    Open questions at the time
    • Preprint, mosquito (non-mammalian) cell context
    • Whether NS1 engages the canonical TPR cargo site unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the affinity hierarchy and phosphorylation status of competing TPR-binding adaptors are integrated to determine cargo selection and transport mode in a given cell remains unresolved.
  • No quantitative competition model across the full adaptor set in vivo
  • Kinases for several functionally relevant phosphosites unidentified
  • Functional consequences of KLC1 splice isoforms on cargo selectivity untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 5 GO:0098772 molecular function regulator activity 3
Localization
GO:0005856 cytoskeleton 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-9609507 Protein localization 4 R-HSA-5653656 Vesicle-mediated transport 3
Partners
CELF1CRMP2DNM1LDOC2BJIP1KIF5AMAP7SFPQ
Complex memberships
kinesin-1 heterotetramer

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 A small 10-amino-acid WD motif in the KLC1 cargo protein Alcadein-α cytoplasmic region is necessary and sufficient to activate kinesin-1 through interaction with the tetratricopeptide repeat (TPR) region of KLC1, promoting vesicular association and anterograde transport; only part of the TPR structure is required for this activation in vivo. In vivo transport assays with artificial transmembrane proteins containing WD motifs, excess KLC1 competition experiments, and domain-deletion analysis of KLC1 TPR region Traffic (Copenhagen, Denmark) High 22404616
2015 KLC1 associates with phagosomes derived from photoreceptor outer segment (POS) disk membranes in the retinal pigment epithelium (RPE) and remains associated during bidirectional microtubule-based movement (including pauses). Loss of KLC1 does not impair phagosome speed but reduces run length and impairs phagosome localization and degradation, leading to AMD-like RPE pathogenesis in aged mice. Live-cell imaging of RPE phagosomes, KLC1 knockout mice with phenotypic analysis including accumulation of RPE/sub-RPE deposits, oxidative and inflammatory stress markers The Journal of cell biology High 26261180
2021 KLC1 acts as a selective adaptor within a tetrameric kinesin complex (KIF5A/KLC1) to bind the RNA-binding protein SFPQ, enabling long-distance axonal transport of SFPQ-RNA granules; this binding is required for axon survival and is disrupted by KIF5A mutations that cause Charcot-Marie Tooth disease. Co-immunoprecipitation of SFPQ with KIF5A/KLC1 complex, genetic loss-of-function (CMT-associated KIF5A mutants), axon degeneration assays, therapeutic rescue experiments The Journal of cell biology High 33284322
2017 Phosphorylation of KLC1 at Thr466 abolishes its conventional interaction with JIP1b and eliminates the enhanced fast velocity (EFV) of APP anterograde transport by kinesin-1, without impairing a separate novel interaction between the central region of JIP1b and the coiled-coil domain of KLC1 that controls efficient high frequency (EHF) of transport. Phosphorylation at Thr466 increases in aged brains, correlating with decreased JIP1 binding to kinesin-1. Site-directed mutagenesis (Thr466Glu phosphomimetic), in vivo transport velocity measurements, co-immunoprecipitation, aged brain biochemistry Molecular biology of the cell High 29093025
2018 Using isothermal titration calorimetry (ITC), seven KLC1 residues in the TPR domain were identified as critical for JIP1 binding; the autoinhibitory LFP-acidic motif of KLC1 marginally inhibits JIP1 binding by overlapping the same footprint; JIP1 and Alcadein-α W-acidic motif compete for the same KLC1-TPR binding site. Isothermal titration calorimetry with truncated KLC1 TPR fragments, mutagenesis of critical KLC1 residues, structural footprinting against published crystal structure of KLC1-TPR:JIP1 complex The Journal of biological chemistry High 30026235
2019 DOC2B is phosphorylated upon insulin stimulation (at Y301), and this phosphorylation enhances its interaction with KLC1; mutation of Y301 in DOC2B blocks insulin-stimulated phosphorylation, abolishes interaction with KLC1, and blunts insulin-stimulated GLUT4 accumulation at the plasma membrane in skeletal muscle cells. Site-directed mutagenesis (Y301 in DOC2B), co-immunoprecipitation, mass spectrometry, skeletal-muscle-specific transgenic mice, GLUT4 plasma membrane accumulation assays Diabetologia High 30707251
2009 Purified AMPK phosphorylates recombinant GST-KLC1 at Ser520 in vitro; however, overexpression of wild-type, phosphomimetic (S517/520D), or non-phosphorylatable (S517/520A) KLC1 mutants produced no difference in glucose-stimulated insulin granule transport dynamics, and no change in KLC1 Ser520 phosphorylation state was detected after AMPK activation. NEGATIVE RESULT: KLC1 phosphorylation at Ser517/520 does not regulate kinesin-1-mediated insulin granule transport. In vitro kinase assay with purified AMPK and recombinant GST-KLC1, overexpression of phosphomutants in MIN6 cells, 3D live-cell spinning disc confocal imaging of granule dynamics, phospho-specific antibody Islets Medium 20074060 21099273
2014 KLC1 physically interacts with the mitochondrial fission protein Dynamin-1-like protein (Dnm1L/DRP1) through its TPR domains, and the two proteins co-localize in cultured cells; Dnm1L does not interact with KIF5 directly, suggesting KLC1 mediates post-fission mitochondrial transport. Yeast two-hybrid screening, co-localization in cultured cells Bioscience, biotechnology, and biochemistry Low 25082190
1993 The human KLC1 gene was cloned; the encoded 569-amino-acid protein contains heptad repeats in the N-terminal domain (typical of cytoskeletal rod domains) and 21-mer repeats in the central and C-terminal domains; the gene was expressed in bacteria and CHO cells and provisionally assigned to chromosome 14q. cDNA cloning and sequencing, bacterial and CHO cell expression, chromosomal mapping DNA and cell biology Medium 8274221
2024 CELF1 protein directly binds KLC1 RNA (demonstrated by CLIP-seq) and down-regulates the splice variant E of KLC1 (KLC1_vE); depletion of CELF1 in cultured cells increases KLC1_vE levels, while overexpression decreases them, establishing CELF1 as a writer controlling KLC1 alternative splicing. CELF1 depletion and overexpression in cultured cells, CLIP-seq database analysis, transcriptomic correlation in human brain samples Biochemical and biophysical research communications Medium 38768546
2024 KLC1 binds CRMP2 in a manner dependent on CRMP2 residue R565 (R566 in zebrafish); the CRMP2 R566C mutation abolishes binding to KLC1 in transfected cultured cells, and knockdown of klc1a in zebrafish produces defective anterior commissure and postoptic commissure formation, phenocopying crmp2 knockdown, establishing a genetic interaction between CRMP2 and KLC1 in forebrain commissure formation. Co-immunoprecipitation in transfected cells (CRMP2 WT vs R566C mutant), zebrafish klc1a morpholino knockdown with commissure formation readout, crmp2 knockdown rescue experiments Developmental neurobiology Medium 38830696
2025 Cryo-EM structure of the autoinhibited kinesin-1 heterotetramer reveals that KLC tetratricopeptide repeat (TPR) domains bind across folded KHC coiled-coils and wedge between KHC motor domains; additionally, KLC C-terminal helices occlude the TPR cargo-binding interfaces, providing a second layer of autoinhibition that directly blocks cargo engagement. Binding of regulatory factors (e.g., MAP7D3) competes with intramolecular KHC coiled-coil interactions to unfurl the autoinhibited structure. Cryo-EM structure determination, crosslinking mass spectrometry validation, functional motility studies, structural modeling bioRxivpreprint High bio_10.1101_2025.07.15.665000
2025 Binding of cargo-adaptor SLiM peptides to the KLC1 TPR domain dislocates the TPR 'shoulder' formed by docking of KHC coiled-coil 1 (CC1) onto the KLC TPR in the autoinhibited complex, freeing motor domains and promoting transition to the open, active state; this opening facilitates binding of the kinesin-1 cofactor MAP7 to the microtubule. Protein design, computational modelling, biophysical analysis (EM), electron microscopy of complete heterotetrameric holoenzyme with and without SLiM peptides bioRxivpreprint Medium bio_10.1101_2025.04.08.647705
2025 In vitro liposome transport assays show that kinesin-1 motors with KLC bound (KinΔC) exhibit autoinhibition on cargo: reduced MT run lengths, lower detachment forces, and ~3-fold lower MT landing rates compared to constitutively active motors; this autoinhibition is reversed by kinesore (a small molecule that overcomes KLC-mediated autoinhibition), demonstrating that cargo-bound KLC maintains partial autoinhibition that fine-tunes transport directionality at 3D microtubule intersections. In vitro liposome transport assay with near-full-length kinesin-1 + KLC, single-MT motility assays, kinesore pharmacological rescue, in silico mechanistic modeling bioRxivpreprint Medium bio_10.1101_2025.05.06.652443
2025 KLC1 interacts with dengue virus NS1 protein (confirmed by proximity ligation and co-immunoprecipitation in Aedes albopictus C6/36 cells); KLC1 decorates NS1-associated vacuoles; silencing KLC1 reduces viral genome synthesis, NS1 secretion, and virus progeny by ~1 log, and disrupts lipid droplet organization, establishing KLC1 as a host susceptibility factor for DENV replication in mosquito cells. Proximity ligation assay, co-immunoprecipitation, transmission immunoelectron microscopy, siRNA silencing, competitive peptide interference, viral titer and genome quantification, lipid droplet imaging bioRxivpreprint Medium 40166163

Source papers

Stage 0 corpus · 27 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 KLC1-ALK: a novel fusion in lung cancer identified using a formalin-fixed paraffin-embedded tissue only. PloS one 196 22347464
2015 Microtubule motors transport phagosomes in the RPE, and lack of KLC1 leads to AMD-like pathogenesis. The Journal of cell biology 68 26261180
2021 Binding and transport of SFPQ-RNA granules by KIF5A/KLC1 motors promotes axon survival. The Journal of cell biology 56 33284322
2012 A small peptide sequence is sufficient for initiating kinesin-1 activation through part of TPR region of KLC1. Traffic (Copenhagen, Denmark) 38 22404616
2019 A role for kinesin-1 subunits KIF5B/KLC1 in regulating epithelial mesenchymal plasticity in breast tumorigenesis. EBioMedicine 33 31204277
1993 Cloning and genetic characterization of the human kinesin light-chain (KLC) gene. DNA and cell biology 27 8274221
2019 DOC2B promotes insulin sensitivity in mice via a novel KLC1-dependent mechanism in skeletal muscle. Diabetologia 22 30707251
2019 Serial liquid biopsies for detection of treatment failure and profiling of resistance mechanisms in KLC1-ALK-rearranged lung cancer. Cold Spring Harbor molecular case studies 22 31753813
2018 Identification of a novel KLC1-ROS1 fusion in a case of pediatric low-grade localized glioma. Brain tumor pathology 21 30350109
2017 Rapid response of brain metastasis to crizotinib in a patient with KLC1-ALK fusion and MET gene amplification positive non-small cell lung cancer: a case report. Cancer biology & medicine 19 28607809
2009 Control of insulin granule dynamics by AMPK dependent KLC1 phosphorylation. Islets 18 21099273
2017 Phosphorylation of KLC1 modifies interaction with JIP1 and abolishes the enhanced fast velocity of APP transport by kinesin-1. Molecular biology of the cell 15 29093025
2016 Hippocampal to basal forebrain transport of Mn2+ is impaired by deletion of KLC1, a subunit of the conventional kinesin microtubule-based motor. NeuroImage 15 27751944
2021 Normal levels of KIF5 but reduced KLC1 levels in both Alzheimer disease and Alzheimer disease in Down syndrome: evidence suggesting defects in anterograde transport. Alzheimer's research & therapy 14 33691783
2010 Cell-wide analysis of secretory granule dynamics in three dimensions in living pancreatic beta-cells: evidence against a role for AMPK-dependent phosphorylation of KLC1 at Ser517/Ser520 in glucose-stimulated insulin granule movement. Biochemical Society transactions 11 20074060
2021 Chronic intermittent hypoxia aggravates skeletal muscle aging by down-regulating Klc1/grx1 expression via Wnt/β-catenin pathway. Archives of gerontology and geriatrics 10 34218156
2023 KLC1-ROS1 Fusion Exerts Oncogenic Properties of Glioma Cells via Specific Activation of JAK-STAT Pathway. Cancers 9 38201436
2018 Characterization of the binding mode of JNK-interacting protein 1 (JIP1) to kinesin-light chain 1 (KLC1). The Journal of biological chemistry 8 30026235
2023 Primary resistance to ALK inhibitors in KLC1/ALK-rearranged pleural metastatic lung adenocarcinoma: a case report. Translational lung cancer research 5 38090529
2014 Dynamin-1-like protein (Dnm1L) interaction with kinesin light chain 1 (KLC1) through the tetratricopeptide repeat (TPR) domains. Bioscience, biotechnology, and biochemistry 5 25082190
2022 Variants in PRKCE and KLC1, Potential Regulators of Type I Psoriasis. Clinical, cosmetic and investigational dermatology 4 35800456
2024 Transcriptome-wide association identifies KLC1 as a regulator of mitophagy in non-syndromic cleft lip with or without palate. iMeta 3 39742305
2016 A molecular dynamics study of the binary complexes of APP, JIP1, and the cargo binding domain of KLC. Proteins 3 27891669
2024 Gene-gene functional relationships in Alzheimer's disease: CELF1 regulates KLC1 alternative splicing. Biochemical and biophysical research communications 2 38768546
2021 The Combined Thermoresponsive Cell-Imprinted Substrate, Induced Differentiation, and "KLC Sheet" Formation. Advanced pharmaceutical bulletin 2 35620328
2024 Forebrain commissure formation in zebrafish embryo requires the binding of KLC1 to CRMP2. Developmental neurobiology 1 38830696
2025 Kinesin light chain 1 (KLC1) interacts with NS1 and is a susceptibility factor for dengue virus infection in mosquito cells. bioRxiv : the preprint server for biology 0 40166163

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