Table 1 Cellular function of mammalian proteins known to interact with DA receptors and the mutant phenotypes of their worm homologues

Function [Reference]

Mutant phenotype [Reference]

Increased D2 receptor stimulation of extracellular signal-regulated kinases and inhibition of adenylate cyclase [41].

cnb-1 mutants show thinner cuticle, decreased brood size and delayed egg laying [43]tax-6 mutants are defective in thermosensation [44]. The specific role of CAL-1 is not known.

Phosphorylation by CaMKII sensitizes D3 receptor [45].

unc-43 mutation lengthens the period of the motor output as well as reduces locomotor activity [46–48].

Desensitization of D2 receptor through calcium sensing [49].

ncs-1 knockout animals show deficits in isothermal tracking behavior [50].

Desensitization through inhibition of D2 receptor-G-protein interaction [23].

arr-1 mutants are defective in olfactory adaptation [51, 52].

Trafficking of D1 and D2 receptors to the cell surface [34].

At 25°C cnx-1 mutants show increased lethality, slow growth, and lower brood size [53].

Cell surface expression and co-localization and stability of D2 receptor subtypes [54].

Not known

Provides scaffold for D2 receptors and relay molecules [42].

nab-1 mutants display reduced synapse density and resistance to paralysis on aldicarb [55].

Regulates D1 cell surface expression, and receptor desensitization [56].

Not known

Adaptor for linking D2-like receptors with cytoskeletal actin [40, 57].

fln-1 mutants have defective spermatheca and reduced brood size [58].

Attenuation of D2 mediated as well as receptor-independent generation of cAMP [59].

lmn-1 mutants show major deficits due to abnormal condensation of chromatin, abnormal distribution of nuclear pore complexes and chromosome loss in some cells [60].

Interaction with D2 receptors potentially regulates chloride channel [61].

The tubular excretory cell lumen in exc-4 mutants is disrupted by swellings similar to cysts found in tubulocystic kidney disease [62, 63].

D2 receptors’ interaction with β-catenin inhibits wnt/calcium signaling pathway [64].

sys-4 mutants display gonadogenesis defects [65].

Internalization of D2 receptors [66].

Not known

D2 interaction enhances TRP1 delivery to cell surface [67].

trp-4 mutants are defective in proprioception and mechanosensation [68, 69].

Attenuates D2 signaling through regulator of G-protein RGS19 [70].

Not known

Transport of D2 receptors to neuronal membrane [71].

RNAi knock-down of T14G10.5 causes defects in locomotion and reduced fertility [72].

Transport of D1 receptors from ER to neuronal membrane [35].

Not known