Gene: T04C12.4   

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 (4)
					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 (5)
	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)
	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

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