ABSTRACT
BACKGROUND: The scalloped (sd) and vestigial (vg) genes function together in Drosophila wing development. Little is known about sd protein (SD) expression during development, or whether sd and vg interact in other developing tissues. To begin to address these questions, we generated an anti-SD antibody. RESULTS: During embryogenesis, SD is expressed in both central and peripheral nervous systems, and the musculature. SD is also expressed in developing flight appendages. Despite SD expression herein, the peripheral nervous system, musculature, and dorsal limb primordia appeared generally normal in the absence of sd function. SD is also expressed in subsets of ventral nerve cord cells, including neuroblast 1-2 descendants and ventral unpaired median motor neurons (mVUMs). While sd function is not required to specify these neurons, it is necessary for the correct innervation of somatic muscles by the mVUMs. We also show that SD and vg protein (VG) are co-expressed in overlapping and distinctive subsets of cells in embryonic and larval tissues. CONCLUSIONS: We describe the full breadth of SD expression during Drosophila embryogenesis, and identify a requirement for sd function in a subset of motor neurons. This work provides the necessary foundation for functional studies regarding the roles of sd during Drosophila development.
Subject(s)
Drosophila Proteins/metabolism , Drosophila melanogaster/embryology , Drosophila melanogaster/metabolism , Transcription Factors/metabolism , Animals , Central Nervous System/embryology , Central Nervous System/metabolism , Drosophila Proteins/genetics , Gene Expression Regulation, Developmental , Imaginal Discs/embryology , Imaginal Discs/metabolism , Muscles/embryology , Muscles/metabolism , Peripheral Nervous System/embryology , Peripheral Nervous System/metabolism , Transcription Factors/geneticsABSTRACT
The Drosophila central nervous system is an excellent model system in which to resolve the genetic and molecular control of neuronal differentiation. Here we show that the wing selector vestigial is expressed in discrete sets of neurons. We track the axonal trajectories of VESTIGIAL-expressing cells in the ventral nerve cord and show that these cells descend from neuroblasts 1-2, 5-1, and 5-6. In addition, along the midline, VESTIGIAL is expressed in ventral unpaired median motorneurons and cells that may descend from the median neuroblast. These studies form the requisite descriptive foundation for functional studies addressing the role of vestigial during interneuron differentiation.
Subject(s)
Central Nervous System/metabolism , Drosophila Proteins/metabolism , Drosophila/metabolism , Nuclear Proteins/metabolism , Animals , Central Nervous System/cytology , Central Nervous System/embryology , Drosophila/cytology , Drosophila/embryology , Embryo, Nonmammalian/cytology , Embryo, Nonmammalian/metabolism , Fluorescent Antibody Technique , Models, Biological , Neurons/cytology , Neurons/metabolismABSTRACT
The adjacent knirps (kni) and knirps-related (knrl) genes encode functionally related zinc finger transcription factors that collaborate to initiate development of the second longitudinal wing vein (L2). kni and knrl are expressed in the third instar larval wing disc in a narrow stripe of cells just anterior to the broad central zone of cells expressing high levels of the related spalt genes. Here, we identify a 1.4 kb cis-acting enhancer element from the kni locus that faithfully directs gene expression in the L2 primordium. We find that three independent ri alleles have alterations mapping within the L2-enhancer element and show that two of these observed lesions eliminate the ability of the enhancer element to direct gene expression in the L2 primordium. The L2 enhancer can be subdivided into distinct activation and repression domains. The activation domain mediates the combined action of the general wing activator Scalloped and a putative locally provided factor, the activity of which is abrogated by a single nucleotide alteration in the ri(53j) mutant. We also find that misexpression of genes in L2 that are normally expressed in veins other than L2 results in abnormal L2 development. These experiments provide a mechanistic basis for understanding how kni and knrl link AP patterning to morphogenesis of the L2 vein by orchestrating the expression of a selective subset of vein-promoting genes in the L2 primordium.
