T04C12.4 | SMap | S_parent | Sequence | T04C12
|
| Chromosome | V |
|
Identity (5)
|
|
Gene_info
| Gene_class | act
|
| |
Allele
| ad767
| Inferred_automatically | From strain object: DA468 |
| | | st22
| Inferred_automatically | From strain object: RW3455 |
| |
Strain
| DA468
|
| | | RW3455
|
| | In_cluster | act-123
|
| |
GO_term
| GO:0003774
| IEA
| Inferred_automatically |
| | | GO:0005200
| IEA
| Inferred_automatically |
| | | GO:0005884
| IEA
| Inferred_automatically |
| | | GO:0005515
| IEA
| Inferred_automatically |
| |
Structured_description
|
Provisional_description
| act-3 encodes an invertebrate actin, highly similar to ACT-1, ACT-2, and ACT-4, that functions in body wall muscle. |
Paper_evidence
| WBPaper00000741
|
| | | | | | WBPaper00001178
|
| | | | | | WBPaper00001709
|
| | | | | | WBPaper00014413
|
| | | | | Person_evidence | WBPerson567
|
| | | | | Curator_confirmed | WBPerson567
|
| | | | | Date_last_updated | 17 Jun 2004 00:00:00 |
| | | | The act-3 gene is embedded in the 11-kb gene cluster act-123. |
| | | | It has one mutant allele act-3(st22), with a slow-moving, fertile heterozygous phenotype and a small, very sick homozygous phenotype; it has its strongest effect on L4 larvae, and, unlike unc-54 alleles that become slower with age, st22 is actually less severe in adults than larvae. |
| | | | Another homozygous viable, dominant act-3 mutation is st15, which phenotypically resembles st22; the alleles st15 and st22 encode the changes T143N and E334K, respectively. |
| | | | act-3(st15) and act-3(st22) alter muscle structure, with particular effects on thin filament arrangement; sarcomeres in st15 and st22 homozygotes are highly disordered. |
| | | | These defects are strongly visible in body wall muscle, but much weaker (st15) or absent (st22) in pharyngeal muscle. |
| | | | Yet another mutant allele of act-3 (ad767) has been isolated on the basis of defective feeding (an Eat phenotype), as part of a double mutant (ad468 ad767) that also mutates act-2. |
| | | | Many ad468 ad767 heterozygotes are slightly starved, indicating semidominance; homozygotes have a strong Phm phenotype, with almost invisible pharyngeal contractions, very slow growth, and very poor fertility (small broods). |
| | | | However, this phenotype does not resemble the act-3(st22) phenotype, and ad468 is the only act-2 allele known; it thus is possible that ad767 is a weak allele of act-3 and that the bulk of the ad468 ad767 phenotype comes from act-2(ad468). |
| | | | The ad468 ad767 phenotype depends on the number of copies of the mutant locus, since ad468 ad767/Df heterozygotes are phenotypically equal to ad468 ad767/+; this suggests that ad468 ad767 causes a gain of function (hypermorph) with toxic effects. |
| | | | ad468 ad767 muscle has birefringence, but the orientation of birefringent fibers varies abnormally from place to place within muscle cells. |
| | | | However, ad468 ad767 homozygotes move normally (unlike act-1 or act-3 mutants). |
| | | Concise_description | act-3 encodes an invertebrate actin, highly similar to ACT-1, ACT-2, and ACT-4, that functions in body wall muscle. |
|
Molecular_info
| Corresponding_CDS | T04C12.4
|
| | Corresponding_protein | WP:CE13148
|
| |
Corresponding_PCR_product (7)
|
| |
Corresponding_RNAi_reagent (13)
|
| |
Other_sequence
| X16796
|
| | | X16798
|
|
Experimental_info
|
RNAi_result
| Cenix:222-b8
|
| | | Cenix:222-d8
|
| | | Simmer:T04C12.4
|
| | | TH:248-g1
|
| |
WB_RNAi_result
| Simmer:M03F4.2
|
| | | Simmer:T04C12.4
|
| | | Simmer:T04C12.5
|
| | | Simmer:T04C12.6
|
| | | Simmer:T25C8.2
|
| | | MV_SV:mv_CAA34717
|
| | | MV_SV:mv_CAA34718
|
| | | MV_SV:mv_M03F4.2
|
| | | Cenix:222-b8
|
| | | TH:248-g1
|
| | | Cenix:222-d8
|
| | | TH:248-h1
|
| | Expr_pattern | Expr6341
|
|
Reference (38)
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Remark
| M03F4.2 connection removed since latter is on another chromosome. [sdm 0107] |
| | T04C12.6 connection removed. email from JAH 0109. |
| | Map position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC. | CGC_data_submission |
| Method | Gene
|