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Hormone‐dependent expression of fasciclin II during ganglionic migration and fusion in the ventral nerve cord of the moth Manduca sexta
Author(s) -
Himes Katherine E.,
Klukas Kathleen A.,
Fahrbach Susan E.,
Mesce Karen A.
Publication year - 2008
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21737
Subject(s) - biology , manduca sexta , microbiology and biotechnology , ventral nerve cord , medicine , endocrinology , central nervous system , botany , larva
The ventral nerve cord of holometabolous insects is reorganized during metamorphosis. A prominent feature of this reorganization is the migration of subsets of thoracic and abdominal larval ganglia to form fused compound ganglia. Studies in the hawkmoth Manduca sexta revealed that pulses of the steroid hormone 20‐hydroxyecdysone (20E) regulate ganglionic fusion, but little is known about the cellular mechanisms that make migration and fusion possible. To test the hypothesis that modulation of cell adhesion molecules is an essential component of ventral nerve cord reorganization, we used antibodies selective for either the transmembrane isoform of the cell adhesion receptor fasciclin II (TM‐MFas II) or the glycosyl phosphatidylinositol‐linked isoform (GPI‐MFas II) to study cell adhesion during ganglionic migration and fusion. Our observations show that expression of TM‐MFas II is regulated temporally and spatially. GPI‐MFas II was expressed on the surface of the segmental ganglia and the transverse nerve, but no evidence was obtained for regulation of GPI‐MFas II expression during metamorphosis of the ventral nerve cord. Manipulation of 20E titers revealed that TM‐MFas II expression on neurons in migrating ganglia is regulated by hormonal events previously shown to choreograph ganglionic migration and fusion. Injections of actinomycin D (an RNA synthesis inhibitor) or cycloheximide (a protein synthesis inhibitor) blocked ganglionic movement and the concomitant increase in TM‐MFas II, suggesting that 20E regulates transcription of TM‐MFas II. The few neurons that showed TM‐MFas II immunoreactivity independent of endocrine milieu were immunoreactive to an antiserum specific for eclosion hormone (EH), a neuropeptide regulator of molting. J. Comp. Neurol. 509:319–339, 2008. © 2008 Wiley‐Liss, Inc.

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