WormBase Tree Display for Variation: WBVar02147648

WBVar02147648 Evidence: Paper_evidence: WBPaper00005832
  Name: Public_name: n3170
  Sequence_details: Mapping_target: Y38C1AA
    Type_of_mutation: Substitution: g a Paper_evidence: WBPaper00005832
    SeqStatus: Pending_curation
  Variation_type: Allele
  Origin: Species: Caenorhabditis elegans
    Laboratory: MT
    Status: Live
  Affects: Gene: WBGene00006561
    Interactor: WBInteraction000538572
  Description: Phenotype: WBPhenotype:0000038 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: Table 1 Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Low: 11 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0006748 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0000414 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "The os14 and n3170 alleles also caused 55% (n = 33) and 45% (n = 31) of Pn.p cells to be missing and 35 and 16% extra Pn.p divisions, respectively. Furthermore, the degree of P12.p-to-P11.p transformation among os14 and n3170 mutants with normal Pn.p numbers was higher than mh15 mutants, 22% and 24%, respectively (Table 2). However, in contrast to mh15 mutants, we did not observe P11.p-to-P12.p cell fate transformations in os14 or n3170 mutants, suggesting that this cell fate transformation might be specific to mh15 mutants." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Incomplete: 24 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0006899 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
            WBbt:0006900 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0000697 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: Table 1 Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Incomplete: 44 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0006748 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0000828 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "Analysis of the T cell lineages showed that the fates of the T.a and T.p cells were variably defective in each tcl-2 mutant (Fig. 1B)." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0004946 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
            WBbt:0004944 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0000839 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "To understand the basis of the gonad defects, we examined Z1 and Z4 cell lineages in six tcl-2(n3170) hermaphrodites. We observed that the divisions of Z1 and Z4 were delayed in all tcl-2 animals. In five tcl-2 animals, Z1 or Z4 divided once before L1 lethargus, and in one Z1 and Z4 started to divide in the early L2 (Fig. 4D), whereas in wild-type animals, Z1 and Z4 divide twice before L1 lethargus (Fig. 4A). In the three animals, the Z1 and Z4 divisions were delayed, but the patterns were the same as wild-type. The remaining three animals displayed loss of division defects shown in Fig. 4B-D." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0004577 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0000840 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "To understand the basis of the gonad defects, we examined Z1 and Z4 cell lineages in six tcl-2(n3170) hermaphrodites. We observed that the divisions of Z1 and Z4 were delayed in all tcl-2 animals. In five tcl-2 animals, Z1 or Z4 divided once before L1 lethargus, and in one Z1 and Z4 started to divide in the early L2 (Fig. 4D), whereas in wild-type animals, Z1 and Z4 divide twice before L1 lethargus (Fig. 4A). In the three animals, the Z1 and Z4 divisions were delayed, but the patterns were the same as wild-type. The remaining three animals displayed loss of division defects shown in Fig. 4B-D." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0004574 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0001355 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "Each tcl-2 allele caused a gonad defect. The os14, os40, and n3170 mutants displayed a similar and more penetrant defect than did mh15 (Table 2)." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Incomplete: 30 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0005175 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0002174 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "The os14 and n3170 alleles also caused 55% (n = 33) and 45% (n = 31) of Pn.p cells to be missing and 35 and 16% extra Pn.p divisions, respectively. Furthermore, the degree of P12.p-to-P11.p transformation among os14 and n3170 mutants with normal Pn.p numbers was higher than mh15 mutants, 22% and 24%, respectively (Table 2). However, in contrast to mh15 mutants, we did not observe P11.p-to-P12.p cell fate transformations in os14 or n3170 mutants, suggesting that this cell fate transformation might be specific to mh15 mutants." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Incomplete: 45 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0006899 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
            WBbt:0006900 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0002175 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: "The os14 and n3170 alleles also caused 55% (n = 33) and 45% (n = 31) of Pn.p cells to be missing and 35 and 16% extra Pn.p divisions, respectively. Furthermore, the degree of P12.p-to-P11.p transformation among os14 and n3170 mutants with normal Pn.p numbers was higher than mh15 mutants, 22% and 24%, respectively (Table 2). However, in contrast to mh15 mutants, we did not observe P11.p-to-P12.p cell fate transformations in os14 or n3170 mutants, suggesting that this cell fate transformation might be specific to mh15 mutants." Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Incomplete: 16 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0006899 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
            WBbt:0006900 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
      WBPhenotype:0002211 Paper_evidence: WBPaper00005832
        Curator_confirmed: WBPerson2987
        Remark: Table 1 Paper_evidence: WBPaper00005832
            Curator_confirmed: WBPerson2987
        Penetrance: Complete: 99 Paper_evidence: WBPaper00005832
              Curator_confirmed: WBPerson2987
        Recessive: Paper_evidence: WBPaper00005832
          Curator_confirmed: WBPerson2987
        EQ_annotations: Anatomy_term: WBbt:0005425 PATO:0000460 Paper_evidence: WBPaper00005832
                Curator_confirmed: WBPerson2987
  Reference: WBPaper00005832
  Method: Substitution_allele