Transcriptional analysis of possible feedback mechanisms of lytic compound production in Alexandrium fundyense


Contact
Sylke.Wohlrab [ at ] awi.de

Abstract

The Harmful Algal Bloom species Alexandrium fundeyense is responsible for outbreaks of paralytic shellfish poisoning in the marine realm of temperate waters. Unknown lytic compounds produced by A. fundeyense are highly discussed to facilitate the formation of these toxic blooms by reducing losses due to competition and grazing. However, avoiding being consumed has to be efficient enough to succeed among other prey organisms. We therefore identified possible feedback mechanisms that A. fundeyense might gain from the lytic compound production on the molecular level. Based on a comprehensive cDNA-library we compared the transcriptional response towards a protistan grazer (Polykrikos kofoidii) of an A. fundeyense strain capable of lytic compound production vs a strain that lacks this ability. We will further highlight genes involved in secondary metabolite synthesis that are differentially expressed between these two strains. Our results strongly suggest that the action of lytic compounds produced by A. fundeyense is associated with an induction of a wide range of cellular functions. Thus, lytic compound production seems to be a trait with more far reaching consequences than only a release from top-down processes. In summary, our results will give novel insights and issues for consideration regarding the autecology of this prominent HAB-species.



Item Type
Conference (Talk)
Authors
Divisions
Primary Division
Programs
Primary Topic
Publication Status
Published
Event Details
The 16th International Conference on Harmful Algae, 27 Oct 2014 - 31 Oct 2014, Wellington, New Zealand.
Eprint ID
39675
Cite as
Wohlrab, S. , Tillmann, U. , Cembella, A. and John, U. (2014): Transcriptional analysis of possible feedback mechanisms of lytic compound production in Alexandrium fundyense , The 16th International Conference on Harmful Algae, Wellington, New Zealand, 27 October 2014 - 31 October 2014 .


Share

Geographical region
N/A

Research Platforms
N/A

Campaigns
N/A


Actions
Edit Item Edit Item