TABLE 4.

Description of the genes that influenced the Twp phenotype

Gene	Protein type	Expression, function, and mutant phenotypes	References
adt-1	ADAMTS protease	Expressed in the head ganglion, ventral nerve cord, vulva, and rays of the male tail. The cn30 allele lacking the protease activity exhibits defects in the formation of the male tail rays.	Kuno et al. (2002)
cle-1	Collagen type XVIII	Present at low levels in all basement membranes but enriched on neurons at synaptic contacts. The cg120 mutant lacks a terminal NC1/endostatin domain and exhibits cell migration and axon guidance defects as well as defective neuromuscular junctions. gk364 and gk421 are superficially wild type according to WormBase.	Ackley et al. (2001),Ackley et al. (2003)
dig-1	Large integral membrane protein	Expressed in muscles, hypodermal cells, and coelomocytes. Mutants exhibit defects in the maintenance of fasciculation and cell-body position, including defects in the positioning of several neurons and of the gonad primordium.	Bénard et al. (2006),Burket et al. (2006)
dpy-7	Cuticle collagen	Expressed by hypodermal cells and forms part of the cuticle that forms the exoskeleton. Mutants have abnormal body form and are typically short and fat.	Johnstone et al. (1992),Gilleard et al. (1997)
fbl-1	Fibulin	Expressed by head muscle cells and intestine, but accumulates on ECM of the pharynx, gonad, and other cells. The mutant exhibits enlarged gonads and has body-shape defects. FBL-1 antagonizes the ADAMTS protease GON-1 during gonad development, and its localization to ECM depends on MIG-17 activity.	Kubota et al. (2004),Hesselson et al. (2004),Kubota et al. (2008)
lam-1	Laminin β	Present in all ECM in C. elegans. Null mutants are lethal. RNAi treatment is also lethal, with embryos failing to properly separate various tissues and pharyngeal muscle cells separating into surrounding tissues.	Kao et al. (2006)
lam-3	Laminin α and γ	Present in all ECM in C. elegans. Null mutants are lethal, with missing or abnormal ECM and defective cell migration and differentiation.	C. C. Huang et al. (2003)
mig-6	Papilin	Transcript is expressed in distal tip cell, body-wall muscles, CAN neurons, and some other cells. Protein is enriched in the ECM of the pharynx, gonad, and intestine. Mutants fall into three allelic classes: mig-6l with defects in the longitudinal migration of the DTCs, mig-6s with defects in the second migration of the DTCs, and mig-6Twp that exhibit twisted pharynges (this study).	Kawano et al. (2009) This study
mig-17	ADAMTS protease	Transcript expressed by body-wall muscles. Protein accumulates on the basement membranes of gonad and pharynx and requires glycosylation for its recruitment to gonad surfaces. Its activity leads to the recruitment of nidogen to the ECM. Mutants have defects in some cell migrations, including DTC migration.	Nishiwaki et al. (2000),Kubota et al. (2004),Nishiwaki et al. (2004),Kubota et al. (2008),Kawano et al. (2009)
mig-23	Membrane-bound nucleoside diphosphatase	Expressed in the pharynx and intestine. It is required for glycosylation and proper localization of MIG-17. The mutant exhibits DTC migration defects similar to mig-17 mutants.	Nishiwaki et al. (2004)
sax-7	L1 CAM homolog	The protein is present in regions of cell–cell contacts during early embryogenesis and later in the nerve ring, nerve cord, pharynx, and gonad. It likely acts as a homo- and heterophilic adhesion molecule. Mutants have defects in blastomere compaction during gastrulation and exhibit embryonic lethality and abnormal neuronal distribution and trajectories.	Sasakura et al. (2005),Wang et al. (2005),Grana et al. (2010)
sup-17	ADAM proteinase orthologous to Drosophila and mouse KUZBANIAN	Activates signaling of NOTCH homolog LIN-12 by cleavage of the ectodomain. Mutants have defects in vulva development as well as in body morphology and male tail development; null alleles are embryonic lethal.	Jarriault and Greenwald (2005),Wen et al. (1997)
unc-52	Basement membrane heparan sulfate proteoglycan Perlecan	Three different isoforms (short, medium, and long) expressed differentially. All isoforms are expressed on muscle surfaces during embryogenesis, and, during late embryogenesis, the short form is enriched in the pharyngeal ECM while the medium form is enriched on body-wall muscles. Null mutants are lethal with defects in the formation of muscle filament lattices. Certain viable alleles have defects in distal tip cell migrations and/or defects in pharyngeal neuron development.	Rogalski et al. (1993),Mullen et al. (1999),Rogalski et al. (2001),Merz et al. (2003),Mörck et al. (2010)
unc-71	ADAM protease	Expressed by the excretory canal cell, the excretory gland, head neurons, and in epidermal cells of the vulva. The protein accumulates on membranes. Mutants have defects in motor axon guidance and sex myoblast migrations.	X. Huang et al. (2003)

DTC, distal tip cell