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Maternal almondex , a neurogenic gene, is required for proper subcellular Notch distribution in early Drosophila embryogenesis
Author(s) -
Das Puspa,
Salazar Jose L.,
LiKroeger David,
Yamamoto Shinya,
Nakamura Mitsutoshi,
Sasamura Takeshi,
Inaki Mikiko,
Masuda Wataru,
Kitagawa Motoo,
Yamakawa Tomoko,
Matsuno Kenji
Publication year - 2020
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/dgd.12639
Subject(s) - notch signaling pathway , biology , notch proteins , hes3 signaling axis , neuroectoderm , microbiology and biotechnology , cell fate determination , signal transduction , transmembrane protein , phenotype , embryonic stem cell , genetics , gene , receptor , mesoderm , transcription factor
Notch signaling plays crucial roles in the control of cell fate and physiology through local cell–cell interactions. The core processes of Notch signal transduction are well established, but the mechanisms that fine‐tune the pathway in various developmental and post‐developmental contexts are less clear. Drosophila almondex , which encodes an evolutionarily conserved double‐pass transmembrane protein, was identified in the 1970s as a maternal‐effect gene that regulates Notch signaling in certain contexts, but its mechanistic function remains obscure. In this study, we examined the role of almondex in Notch signaling during early Drosophila embryogenesis. We found that in addition to being required for lateral inhibition in the neuroectoderm, almondex is also partially required for Notch signaling‐dependent single‐minded expression in the mesectoderm. Furthermore, we found that almondex is required for proper subcellular Notch receptor distribution in the neuroectoderm, specifically during mid‐stage 5 development. The absence of maternal almondex during this critical window of time caused Notch to accumulate abnormally in cells in a mesh‐like pattern. This phenotype did not include any obvious change in subcellular Delta ligand distribution, suggesting that it does not result from a general vesicular‐trafficking defect. Considering that dynamic Notch trafficking regulates signal output to fit the specific context, we speculate that almondex may facilitate Notch activation by regulating intracellular Notch receptor distribution during early embryogenesis.