290
senescence molecules. The bacterium is thought to detect aging in its algal host
through production of cell wall breakdown products, which trigger production of
compounds called roseobacticides that can act as potent algicides (Seyedsayamdost
et al. 2011b). Another roseobacter, Silicibacter sp. strain TM1040, is also thought to
produce an algicidal molecule known as roseobacter motility inducer (RMI), which
causes death in the chlorophyte Tetraselmis (Sule and Belas 2013). The production
of these compounds is stimulated by the proposed senescence molecule p-coumaric
acid (p-CA) (Seyedsayamdost et al. 2011a, b, 2014; Sule and Belas 2013), an intermediary of lignin biosynthesis (Schaefer et al. 2008; Weng and Chapple 2010).
Roseobacticides are assembled from the bacterially produced phenylacetic acid
(PAA), algal pCA and cysteine derived from algal DMSP (Sule and Belas 2013;
Seyedsayamdost et al. 2014), linked to TDA biosynthesis and regulated by QS AHL
signals (Wang et al. 2016). These roseobacticides are of interest as they demonstrate
a highly specific activity. When tested against selected haptophytes, a green alga, a
diatom and a cryptomonad, only the E. huxleyi culture was completely killed by
roseobacticides, and a third of the cryptomonad Rhodomonas salina cells was
killed. The diatom Chaetoceros muelleri demonstrated morphological changes in
response to the roseobacticide (Seyedsayamdost et al. 2011b). This targeted activity,
such as cell lysis resulting in the release of internal compounds, can be useful for
commercial processing.
The fact that P. gallaeciensis responds to algal p-CA, a lignin intermediary, is an
evolutionary puzzle; lignin is a complex and highly recalcitrant form of carbon
often thought to be one of the key evolutionary advancements allowing the movement of plants from marine habitats to terrestrial ecosystems, essential for structural
support and water retention (Boerjan et al. 2003; Weng and Chapple 2010). The
discovery of lignin and its intermediates in algae presents the intriguing possibility
that these intermediates may have an alternate role as signalling molecules (Schaefer
et al. 2008; Martone et al. 2009; Seyedsayamdost et al. 2011b; Goiris et al. 2014;
Labeeuw et al. 2015). This is consistent with the theory that lignin and its intermediates may form an ancient microbial defence system of plants and algae against
bacteria (Boudet 2000; Tronchet et al. 2010; Labeeuw et al. 2015).
Segev et al. (2016) propose that IAA is another metabolite involved in both the
symbiotic and pathogenic phase of the P. inhibens DSM 17395 and E. huxleyi interaction. However, it should be noted that the concentration at which IAA becomes
algicidal (1000 μM) is much higher than any marine bacteria which is currently
known to be produced (e.g. 10 nM) (Maruyama et al. 1989; Xie et al. 1996;
Fernandes et al. 2011). Concentrations of 100 μM have been shown to be detrimental to the health of algae (Bajguz and Piotrowska-Niczyporuk 2013; Labeeuw et al.
2016), while even in plants, concentrations of IAA above 200 μM are lethal (Baker
and Ray 1965). It remains to be demonstrated that IAA is algicidal at biologically
relevant concentrations. The IAA precursor tryptophan was also shown to be
algicidal at that high concentration (1000 μM) (Labeeuw et al. 2016). Interestingly,
IAA production was lower in the coculture of the pathogenic Ruegeria sp. R11 on
the coccolith-bearing strain of E. huxleyi (which was shown to produce IAA in
L. Labeeuw et al.
senescence molecules. The bacterium is thought to detect aging in its algal host
through production of cell wall breakdown products, which trigger production of
compounds called roseobacticides that can act as potent algicides (Seyedsayamdost
et al. 2011b). Another roseobacter, Silicibacter sp. strain TM1040, is also thought to
produce an algicidal molecule known as roseobacter motility inducer (RMI), which
causes death in the chlorophyte Tetraselmis (Sule and Belas 2013). The production
of these compounds is stimulated by the proposed senescence molecule p-coumaric
acid (p-CA) (Seyedsayamdost et al. 2011a, b, 2014; Sule and Belas 2013), an intermediary of lignin biosynthesis (Schaefer et al. 2008; Weng and Chapple 2010).
Roseobacticides are assembled from the bacterially produced phenylacetic acid
(PAA), algal pCA and cysteine derived from algal DMSP (Sule and Belas 2013;
Seyedsayamdost et al. 2014), linked to TDA biosynthesis and regulated by QS AHL
signals (Wang et al. 2016). These roseobacticides are of interest as they demonstrate
a highly specific activity. When tested against selected haptophytes, a green alga, a
diatom and a cryptomonad, only the E. huxleyi culture was completely killed by
roseobacticides, and a third of the cryptomonad Rhodomonas salina cells was
killed. The diatom Chaetoceros muelleri demonstrated morphological changes in
response to the roseobacticide (Seyedsayamdost et al. 2011b). This targeted activity,
such as cell lysis resulting in the release of internal compounds, can be useful for
commercial processing.
The fact that P. gallaeciensis responds to algal p-CA, a lignin intermediary, is an
evolutionary puzzle; lignin is a complex and highly recalcitrant form of carbon
often thought to be one of the key evolutionary advancements allowing the movement of plants from marine habitats to terrestrial ecosystems, essential for structural
support and water retention (Boerjan et al. 2003; Weng and Chapple 2010). The
discovery of lignin and its intermediates in algae presents the intriguing possibility
that these intermediates may have an alternate role as signalling molecules (Schaefer
et al. 2008; Martone et al. 2009; Seyedsayamdost et al. 2011b; Goiris et al. 2014;
Labeeuw et al. 2015). This is consistent with the theory that lignin and its intermediates may form an ancient microbial defence system of plants and algae against
bacteria (Boudet 2000; Tronchet et al. 2010; Labeeuw et al. 2015).
Segev et al. (2016) propose that IAA is another metabolite involved in both the
symbiotic and pathogenic phase of the P. inhibens DSM 17395 and E. huxleyi interaction. However, it should be noted that the concentration at which IAA becomes
algicidal (1000 μM) is much higher than any marine bacteria which is currently
known to be produced (e.g. 10 nM) (Maruyama et al. 1989; Xie et al. 1996;
Fernandes et al. 2011). Concentrations of 100 μM have been shown to be detrimental to the health of algae (Bajguz and Piotrowska-Niczyporuk 2013; Labeeuw et al.
2016), while even in plants, concentrations of IAA above 200 μM are lethal (Baker
and Ray 1965). It remains to be demonstrated that IAA is algicidal at biologically
relevant concentrations. The IAA precursor tryptophan was also shown to be
algicidal at that high concentration (1000 μM) (Labeeuw et al. 2016). Interestingly,
IAA production was lower in the coculture of the pathogenic Ruegeria sp. R11 on
the coccolith-bearing strain of E. huxleyi (which was shown to produce IAA in
L. Labeeuw et al.