Identification of cis-Regulatory Region Controlling Semaphorin-1a Expression in the Drosophila Embryonic Nervous System
Young Gi Hong1, Bongsu Kang1,2, Seongsoo Lee3, Youngseok Lee4, Bong-Gun Ju5, and Sangyun Jeong1,2,*
1Division of Life Sciences (Molecular Biology Major), Jeonbuk National University, Jeonju 54896, Korea, 2Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Jeonbuk National University, Jeonju 54896, Korea, 3Gwangju Center, Korea Basic Science Institute, Gwangju 61186, Korea, 4Department of Bio and Fermentation Convergence Technology, BK21 PLUS Project, Kookmin University, Seoul 02707, Korea, 5Department of Life Science, Sogang University, Seoul 04107, Korea
Received November 26, 2019; Revised December 19, 2019; Accepted December 20, 2019.; Published online February 6, 2020.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

The Drosophila transmembrane semaphorin Sema-1a mediates forward and reverse signaling that plays an essential role in motor and central nervous system (CNS) axon pathfinding during embryonic neural development. Previous immunohistochemical analysis revealed that Sema-1a is expressed on most commissural and longitudinal axons in the CNS and five motor nerve branches in the peripheral nervous system (PNS). However, Sema-1a-mediated axon guidance function contributes significantly to both intersegmental nerve b (ISNb) and segmental nerve a (SNa), and slightly to ISNd and SNc, but not to ISN motor axon pathfinding. Here, we uncover three cis -regulatory elements (CREs), R34A03, R32H10, and R33F06, that robustly drove reporter expression in a large subset of neurons in the CNS. In the transgenic lines R34A03 and R32H10 reporter expression was consistently observed on both ISNb and SNa nerve branches, whereas in the line R33F06 reporter expression was irregularly detected on ISNb or SNa nerve branches in small subsets of abdominal hemisegments. Through complementation test with a Sema1a loss-of-function allele, we found that neuronal expression of Sema-1a driven by each of R34A03 and R32H10 restores robustly the CNS and PNS motor axon guidance defects observed in Sema-1a homozygous mutants. However, when wild-type Sema-1a is expressed by R33F06 in Sema1a mutants, the Sema-1a PNS axon guidance phenotypes are partially rescued while the Sema-1a CNS axon guidance defects are completely rescued. These results suggest that in a redundant manner, the CREs, R34A03, R32H10, and R33F06 govern the Sema-1a expression required for the axon guidance function of Sema-1a during embryonic neural development.
Keywords: axon guidance, cis-regulatory element, Drosophila, motor neurons, semaphorin-1a
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31 January 2020 Volume 43,
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