Involvement of a novel p38 mitogen-activated protein kinase in larval metamorphosis of the polychaete Hydroides elegans (Haswell)

✍ Scribed by Hao Wang; Pei-Yuan Qian

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 366 KB
• Volume: 314B
• Category: Article
• ISSN: 1552-5007
• DOI: 10.1002/jez.b.21344

✦ Synopsis

Abstract

Hydroides elegans is a common marine fouling organism in most tropical and subtropical waters. The life cycle of H. elegans includes a planktonic larval stage in which swimming larvae normally take 5 days to attain competency to settle. Larval metamorphosis marks the beginning of its benthic life; however, the endogenous molecular mechanisms that regulate metamorphosis remain largely unknown. In this study, a PCR‐based suppressive subtractive hybridization (SSH) library was constructed to screen the genes expressed in competent larvae but not in precompetent larvae. Among the transcripts isolated from the library, 21 significantly matched sequences in the GenBank. Many of these isolated transcripts have putative roles in the reactive oxygen species (ROS) signal transduction pathway or in response to ROS stress. A putative novel p38 mitogen‐activated protein kinase (MAPK), which was also isolated with SSH screen, was then cloned and characterized. The MAPK inhibitors assay showed that both p38 MAPK inhibitors SB202190 and SB203580 effectively inhibited the biofilm‐induced metamorphosis of H. elegans. A cell stressors assay showed that H~2~O~2~ effectively induced larval metamorphosis of H. elegans, but the inductivity of H~2~O~2~ was also inhibited by both SB inhibitors. The catalase assay showed that the catalase could effetely inhibit H. elegans larvae from responding to inductive biofilm. These results showed that the p38 MAPK‐dependent pathway plays critical role in controlling larval metamorphosis of the marine polychaete H. elegans, and the reactive oxygen radicals produced by biofilm could be the cue inducing larval metamorphosis. J. Exp. Zool. (Mol. Dev. Evol.) 314B:390–402, 2010. © 2010 Wiley‐Liss, Inc.