Disease relevance of nau

• Both methods produced a range of defects that included embryonic muscle disruption, reduced viability and female sterility, which could be rescued by hsp70-nautilus cDNA transgenes [1].

High impact information on nau

• Examination of earlier events of muscle development indicates that the specification and early differentiation of somatic muscle precursors are not affected because even-skipped-, nautilus-, and beta 3-tubulin-expressing myoblasts are present [2].
• These observations establish nau as the earliest known marker of myogenesis in Drosophila and indicate that this gene may be a key determinant of pattern formation in the embryonic mesoderm [3].
• Subsequently, nau transcripts are present in at least a subset of growing muscle precursors and mature muscle fibers that exhibit distinct segmental differences [3].
• These early nau-positive cells are detected just prior to the first morphological evidence of muscle cell fusion and occupy similar positions as the later-appearing muscle precursors [3].
• Our results demonstrate Nautilus expression marks early founders that give rise to diverse muscle groups in the embryo, and that nautilus gene activity is required to seed the correct founder myoblast pattern that prefigures the muscle fiber arrangement during embryonic development [1].

Biological context of nau

• The muscle founder cell marker Duf-LacZ, produced by the enhancer trap line rP298LacZ, is coexpressed in numerous Nautilus-positive cells when founders first appear [1].
• In previous studies, the nau zygotic loss-of-function phenotype was determined using genetic deficiencies in which the gene is deleted [4].
• Low-stringency hybridizations indicate that Dmyd is not a member of a multigene family similar to MyoD in vertebrates [5].
• Dmyd clone encodes a polypeptide of 332 amino acids with 82% identity to MyoD in the 41 amino acids of the putative helix-loop-helix region and 100% identity in the 13 amino acids of the basic domain proposed to contain the essential recognition code for muscle-specific gene activation [5].
• RNA interference demonstrates a role for nautilus in the myogenic conversion of Schneider cells by daughterless [6].

Anatomical context of nau

• We show that ventral ectoderm induces mesoderm cells to express nautilus (a MyoD homologue) and to differentiate somatic myofibers, whereas dorsal ectoderm induces mesoderm cells to express visceral and cardiac muscle-specific genes [7].

Regulatory relationships of nau

• Using the GAL4/UAS system, we demonstrate that the wg-derived signal can originate from either ectoderm or mesoderm to influence nau expression [8].

Other interactions of nau

• Full-length RT-PCR products for nautilus and DMEF2 encode immunoprecipitable proteins [6].
• Genetic and molecular characterization of two overlapping deficiencies, Df(3R)nau-9 and Df(3R)nau-11a4, revealed that both of these deficiencies remove the nautilus gene without affecting a common lethal complementation group [9].

Analytical, diagnostic and therapeutic context of nau

• We inactivated the nautilus gene using homology-directed gene targeting and Gal4/UAS regulated RNAi to determine whether loss of nautilus gene activity affected founder cell function [1].

References