Laboratory Information

NameMH View on WormBase
Allele designationku
HeadMin Han
InstitutionUniversity of Colorado at Boulder
Address University of Colorado
Boulder 80309
United States
Gene classes acs  ain  dli  ect  glv  ksr  mek  mnp  nprl  rho  rrp  slr  sptl  sur 
disl  vglm  vgln  dbt  ate  cerk  dus  fath 

Strains contributed by this laboratory

Strain Genotype Species Description
MH1019 soc-2(ku167) IV. C. elegans No obvious phenotype alone. ku167 suppresses let-60(n1046). Previously called sur-8.
MH1113 dpy-20(e1282) IV; sur-5(ku74) X. C. elegans Dpy.
MH1131 soc-2(ku167) let-60(n1046) IV. C. elegans Less than 5% Muv. Previously called sur-8(ku167).
MH1152 egl-26(ku228) II. C. elegans 83% Egl. 4% Sterile.
MH1157 him-5(e1490) V; egl-13(ku194) X. C. elegans ku194 is a loss of function allele, likely to be molecular null. Connection of gonad defective, >95% Egl. Anchor cell and uterine seam cell do not fuse. Males can mate. Hermaphrodites are very difficult to mate. Previously called cog-2(ku194).
MH1292 sur-6(ku123) I. C. elegans Weak Vul phenotype. Suppressor of gain-of-function Ras. ku123 causes a C302Y substitution.
MH1301 unc-83(ku18) V. C. elegans Point mutation W257-> stop codon. Disrupts P cell nuclear migration at 25C. This leads to an Egl, Unc worm. P cell nuclear migration is normal at 15C. hyp7 nuclear migration is normal at all temperatures.
MH1317 kuIs29 V. C. elegans kuIs29 [egl-13p::GFP + unc-119(+)] V. egl-13 is the new gene name for cog-2. Transcriptional fusion of GFP to egl-13 gene. Nuclear localized. Bright expression in body wall muscles, expressed in uterine pi lineage, extensive neuronal expression. Note that a very low penetrance Cog phenotype is seen in this strain. Transgenes with egl-13 promoter can cause Cog phenotype. Conflicting map data: Wendy Hanna-Rose mapped kuIs129 to the left of dpy-11; Shi lab reported it close to gon-10 and unc-76.
MH1346 kuIs35. C. elegans kuIs35 [sem-4::GFP].
MH1564 kuIs36 II. C. elegans kuIs36 [egl-26::GFP + unc-119(+)] II. Transcriptional fusion of GFP to egl-26 gene. Nuclear localized. Embryonic expression. Expressed in somatic gonad (uterus and spermatheca) and vulva in vulE and vulB in L4. Spermatheca expression persists into adulthood. Expressed in pharyngeal-intestinal junction cells and in tail.
MH17 sur-2(ku9) I. C. elegans 100% bag of worms. Low percentage of dead larvae. Slightly dumpy. ku9 completely suppresses let-60(n1046) Muv phenotype.
MH1914 lin-40(ku285) V. C. elegans Animals grow slowly and are semi-sterile. Vulval lineage defective.
MH1946 dli-1(ku266)/+ IV; him-5(e1490) V. C. elegans Heterozygotes are WT and segregate WT and Sterile animals with a protruding vulva. Throws males. Clone several WT to recover heterozygote. Cytoplasmic dynein light intermediate chain. 9/02: ku266 is not an L to stop; it is a W117 to a stop (TGG to TGA). Sandhya Koushika.
MH1955 nhr-25(ku217) X. C. elegans Temperature sensitive Egl.
MH2051 kuIs55. C. elegans kuIs55 [lon-3::GFP + unc-119(+)]. Rollers. The kuIs55 lon-3::GFP transgene does not rescue the Lon phenotype of lon-3 mutants, but instead causes an adult Rol (Roller) phenotype both in lon-3 mutants and in wild-type backgrounds. Reference: Suzuki Y, et al. 2002. Genetics 162: 1631–1639.
MH2211 unc-29(e1072); sur-6(ku123); kuIs57. C. elegans kuIs57 [col-10p::lin-45(gf) + sur-5::GFP]. Reference: Yoder JH, et al. EMBO J. 2004 Jan 14;23(1):111-9.
MH2230 dph-3(ku432) . C. elegans Superficially wild type. Maintain under standard conditions. Reference: Kims S, et al. Genetics. 2010 Aug;185(4):1235-47.
MH2285 lin-66(ku423) IV/nT1 [unc-?(n754) let-?] (IV;V). C. elegans Heterozygotes are Unc. ku423 homozygotes have delayed heterochronic phenotype and are L4 lethal.
MH2294 scc-3(ku263)/lin-25(n545) V. C. elegans Heterozygotes are WT and segregate WT, lin-25 homozygotes (which are temperature sensitive: at 25C adult hermaphrodites are vulvaless, at 15C 8% of adult hermaphrodites are vulvaless), and scc-3 homozygotes which are Pvl and Sterile (vulval morphogenesis defects and defects in sister-chromatin cohesion).
MH231 let-60(n1046) IV; ksr-1(ku68) X. C. elegans Semi-dominant suppressor of let-60(n1046). Strong reduction of function mutation. At 20C: <1% Muv, 24% Egl, 6% larval lethal, and SM migration defects.
MH2354 swsn-1(ku355) V. C. elegans Synthetic lethal with lin-35(n745). Temperature sensitive.
MH2385 ain-1(ku322) X. C. elegans WT looking worms. 40% alae gap. ku322 suppresses lin-31(lf) Muv phenotype. Received new stock 8/2006 from Han lab.
MH2407 ect-2(ku427) II. C. elegans Bag. Missing Pn.p cell.
MH2430 cbp-1(ku258) III. C. elegans Semidominant suppressor of let-60(n1046).
MH2805 kuIs70. C. elegans kuIs70 [alr-1p::GFP + rol-6(su1006)]. Rollers. alr-1p::GFP expression is visible in embryonic and adult tissues. Reference: Tucker M, et al. Mol Biol Cell. 2005 Oct;16(10):4695-704.
MH3084 ain-2(tm1863) I; ain-1(ku322) X. C. elegans Double mutants displayed a severe defect in seam-cell development, implicating a retarded heterochronic phenotype. Protruding vulva phenotype. Increased number of seam cells. Reference: Zhang L, et al. Mol Cell. 2007 Nov 30;28(4):598-613. PMID: 18042455
MH351 let-60(sy101sy127)/dpy-20(e1282) IV. C. elegans Heterozygotes are WT and segregate WT, Dpys and lethals.
MH37 mpk-1(ku1) unc-32(e189) III. C. elegans Unc. ku1 pka sur-1(ku1).
MH4176 ain-1(ku425) X. C. elegans Superficially wild-type. Identified in a screen for suppressors of the Multivulva (Muv) phenotype in lin-31 loss-of-function (lf) mutants. Reference: Ding L, et al. Mol Cell. 2005 Aug 19;19(4):437-47. PMID: 16109369.
MH4177 ain-1(tm3681) X. C. elegans Developmental timing delay. Maintain under normal conditions. Reference: Zhang X, et al. PNAS. 2011 Nov 1;108(44):17997-8002.
MH4429 ain-2(tm2432) I. C. elegans Superficially wild-type. Maintain under normal conditions. Reference: Zhang X, et al. PNAS. 2011 Nov 1;108(44):17997-8002.
MH4799 elt-1(ku491) IV. C. elegans Reference: Cohen ML, et al. PLoS Genet. 2015 Mar 27;11(3):e1005099.
MH4810 elt-1(ku491) IV; wIs51 V; daf-12(rh61rh411) X; kuEx194. C. elegans wIs51 [SCMp::GFP + unc-119(+)] V. kuEx194 [elt-1(+) + sur-5p::DsRed]. GFP expression in seam cells. Pick DsRed+ animals to maintain. In a daf-12(WT) background, elt-1(ku491) exhibits some precocious fusion of seamcells and gaps in alae. elt-1(ku491); daf-12(rh61rh411) double mutants have more sever heterochronic phenotypes including seamcell proliferation and bursting vulvae. Reference: Cohen ML, et al. PLoS Genet. 2015 Mar 27;11(3):e1005099.
MH4920 unc-119(ed3) III; kuIs102. C. elegans kuIs102 [vgln-1p::vgln-1::GFP + Cbr-unc-119(+)]. Integrated translational VGLN-1::GFP fusion protein. Reference: Zabinsky RA, et al. G3 (Bethesda). 2017 Jun 2. pii: g3.117.043414. doi: 10.1534/g3.117.043414. PMID: 28576776
MH5015 kuIs118 II; unc-119(ed3) III. C. elegans kuIs118 [daf-15p::daf-15::mCherry + Cbr-unc-119(+)] II. kuIs118 is a single copy insertion into ttTi5605 via CRISPR/Cas9. Superficially wild-type. mCherry expression observed throughout the body. mCherry detected throughout development by western blot with anti-mCherry antibody, with highest expression levels in early larval stages. Reference: Sewell AK, et al. "The TORC1 phosphoproteome in C. elegans reveals roles in transcription and autophagy” iScience, 20 May 2022, 104186.
MH5197 nprl-3(ku540) IV. C. elegans Superficially wildtype. Homozygous nprl-3(ku540) can suppress the early larval arrest phenotype of mmBCFA deficiency mutants elo-5(gk208) and cgt-1(tm1027) cgt-3(tm504). References: Zhu H, et al. Elife. 2013 May 21;2:e00429. Zhu H, Sewell AK, Han M. Genes Dev. 2015 Jun 15;29(12):1218-23.
MH5239 prx-5(ku517) II. C. elegans Suppresses the developmental arrest of elo-5(gk208). Slightly delayed development/growth.
MH538 mek-2(ku114) I; let-60(n1046) IV. C. elegans
MH734 ksr-1(ku68) X. C. elegans At 20C: 7% Egl, 22% larval lethal. Vulval lineages WT.
MH801 sur-7(ku119) X. C. elegans No obvious morphological phenotype on its own. Good suppressor of Muv of let-60(n1046).
OP50/cytR- E. coli [cytR-] Escherichia coli Bacteria. Kanamycin-resistant E. coli. cytR- mutation in OP50 background causes elavated nucleotide levels similar to HT115. A mutation in CytR- was introduced into the OP50 strain by recombineering. Bacterial cells were transformed with pSIM8 plasmid before using as hosts for recombineering. Targeting substrate DNA fragments were amplified by PCR and subcloned into TOPO cloning vector for sequence verification before being electroporated into the host bacterial cells. The primer set used for cloning targeting cytR substrate DNAs (to replace cytR+ with the cytR- mutation identified in HT115 strain): 5'- GCCAGGCGAGGAGTGAGTGTG-3'/5'-AGCGGCGGGCCTTTGACC-3'. Reference: Chi C, et al. Genes Dev. 2016 Feb 1;30(3):307-20.

Alleles contributed by this laboratory

Allele Type DNA Change Protein Change
ku167 Allele substitution
ku212 Allele
ku74 Allele
ku228 Allele substitution
ku194 Allele substitution nonsense
ku123 Allele substitution
ku18 Allele
ku9 Allele substitution nonsense
ku298 Allele substitution
ku285 Allele substitution splice_site
ku266 Allele
ku217 Allele substitution
ku156 Allele
ku432 Allele deletion
ku423 Allele substitution nonsense
ku263 Allele substitution nonsense
ku68 Allele substitution
ku355 Allele
ku322 Allele substitution nonsense
ku427 Allele substitution
ku258 Allele substitution
ku1 Allele
ku491 Allele substitution
ku540 Allele substitution
ku114 Allele substitution slient
ku51 Allele substitution
ku112 Allele substitution
ku119 Allele substitution splice_site
ku233 Allele substitution
ku354 Allele substitution