Table 2.

Summary of myofibril assembly and thin filament length phenotypes in Tmod1 perturbation experiments.

Perturbation	Model system	Experimental strategy	Resulting phenotype	References
Reduced Tmod1 levels	Mouse embryonic heart	Gene knockout	Myofibril disorganization, nonstriated actin	[59, 65, 68]
	Mouse embryonic stem cells	Gene knockout	Myofibril disorganization, nonstriated actin	[69]
	Mouse skeletal muscle	Gene knockout	No effect*	[31]
	Rat cardiomyocytes	Antisense cDNA expression	Thin filament elongation, nonstriated actin	[70]
	Drosophila primary muscle cells**	RNAi knockdown	Sarcomere length irregularity, thin filament elongation	[71]
	C. elegans body wall muscle***	RNAi knockdown, unc94/tmd-1 mutant alleles	Myofibril disorganization, nonstriated actin, myofibril attachment defects	[14, 15]
Inhibition of Tmod1 function	Chick cardiomyocytes	Antibody inhibition of actin capping	Thin filament elongation, nonstriated actin	[28]
	Chick cardiomyocytes	Antibody inhibition of TM binding	Thin filament disassembly	[41]
Tmod1 overexpression	Chick cardiomyocytes	cDNA expression	Thin filament shortening	[29]
	Rat cardiomyocytes	cDNA expression	Myofibril disorganization, thin filament shortening	[70]
	Adult mouse heart	α-Myosin heavy chain promoter-driven Tmod1 transgene	Myofibril disorganization, thin filament shortening, intercalated disc defects	[72]
	Drosophila indirect flight muscle**	HSP-90-driven Tmod transgene	Thin filament shortening	[13]
	Drosophila primary muscle cells**	Dmef-GAL4, UAS-Tmod transgene	Thin filament shortening	[71]

*No myofibril assembly or thin filament length alterations occur in Tmod1-null mouse skeletal muscle, but extrasarcomeric SR defects do occur due to Tmod3 translocation from the SR to the thin filament pointed ends.

**Drosophila Tmod was knocked down or overexpressed.

***C. elegans UNC94/TMD-1 was knocked down or overexpressed.