Table 1.

Function of actin-binding proteins (ABPs) based on studies of genetic models and mutation analysis

ABP	Mr (kDa)	Phenotypes
Arp3	45	Embryos of Arp3 deficient mice failed to develop beyond blastocysts stage [31].
Eps8	97	Eps8 null mice were normal and fertile [32]. Length of intestinal microvilli in Eps8 KO vs. WT mice reduced by 25%, leading to significant reduction in intestinal fat absorption [33]. Effects on ES unknown.
Ezrin	85	Ezrin mutation mouse pups died before weaning, defects in epithelial organization and villus morphogenesis were observed in the gastrointestinal tract [34,35].
Fascin 1	54	Fascin 1 deficient mice were viable and fertile without major developmental defects except neurons exhibited fewer and shorter filopodia vs. WT [36]. Embryonic fibroblasts lacking fascin 1 also displayed fewer and shorter filopodia and were short-lived [36].
Filamin A	280	Filamin A-deficient mice led to embryonic leathality due to severe hemorrhage and cardiac structural defects [37]. Thus, its effects following KO on the testis remain unknown.
Palladin	95	Loss of palladin results in embryonic lethality, embryos died at E15.5 due to cranial neural tube closure defects (NTDs) and herniation of liver and intestine [38].
Rai14	110	Mutation of Rai14 via its deletion led to a complex neurobehavioral disorder known as Smith-Magenis syndrome (SMS) in humans [39,40], associated with schizophrenia [41] and spinocerebellar ataxia type 2 (SCA2) [42]. Its duplication led to autism [43] and Potocki-Lupski syndrome [44].