Targeted deletion of the ATP binding domain of left-right dynein confirms its role in specifying development of left-right asymmetries.

ABSTRACT: Vertebrates develop distinct asymmetries along the left-right axis, which are consistently aligned with the anteroposterior and dorsoventral axes. The mechanisms that direct this handed development of left-right asymmetries have been elusive, but recent studies of mutations that affect left-right development have shed light on the molecules involved. One molecule implicated in left-right specification is left-right dynein (LRD), a microtubule-based motor protein. In the LRD protein of the inversus viscerum (iv) mouse, there is a single amino acid difference at a conserved position, and the lrd gene is one of many genes deleted in the legless (lgl) mutation. Both iv and lgl mice display randomized left-right development. Here we extend the analysis of the lrd gene at the levels of sequence,

SUBMITTER: Supp DM 

PROVIDER: S-EPMC1797880 | biostudies-literature | 1999 Dec

REPOSITORIES: biostudies-literature