289
Pseudoalteromonas piscicida was found to be a potent algicidal molecule causing
the death of E. huxleyi (Harvey et al. 2016). The bacterium Alteromonas sp. was
isolated from a harmful algal bloom, and four compounds (2-undecen-1′-yl-4quinolone, 2-undecyl-4-quinolone, 3-hexyl-6-pentyl-4-hydroxyl-2H-pyran-2-one
and 6-heptyl-3-hexyl-4-hydroxyl-2H-pyran-2-one) were isolated which had specific activity against harmful dinoflagellates but had a lower activity against other
microalgae (Cho 2012). Two algicidal compounds, prolyl-methionine and hypoxanthine, were identified from a bacterium Bacillus sp. which was isolated from a
bloom of the haptophyte Phaeocystis globosa; they were found to target antioxidant
systems within the alga (Yang et al. 2015). Lactones produced by Ruegeria pomeroyi were found to target and harm only the algae (Chlorella fusca) when tested
against other bacteria, fungi and the alga (Riclea et al. 2012). In addition to algicidal
molecules, bacteria can also produce molecules that negatively affect the behaviour
of algae. Anatoxin-a and microcystin-LR are two toxins produced by cyanobacteria
that can inhibit motility in the chlorophyte Chlamydomonas reinhardtii and cause
increased settling and sinking of the alga (Kearns and Hunter 2001).
Algae have developed a suite of small molecules that can act as chemical
defences, which they can deploy to inhibit colonization, organisms competing for
available resources or predators (Hay 1996; Wolfe et al. 1997; Potin et al. 2002;
Steinberg and de Nys 2002). For example, (macro) brown algae produce phlorotannins which are potent antimicrobial metabolites against a range of bacteria, fungi
and other algae (Eom et al. 2012). Likewise, microalgae have been shown to produce antibiotic compounds. Various diatoms produce polyunsaturated aldehydes
(PUA) which can inhibit various bacteria (conversely, it was also found to stimulate
a few specific species of bacteria as well) (Ribalet et al. 2008).
One of the most studied chemical defence systems has been in the (macro) red
algae Delisea pulchra, which is subject to bleaching due to various bacterial pathogens (Case et al. 2011; Kumar et al. 2016). The macroalga can release furanones,
similar in structure to the QS AHL molecules, thereby inhibiting the bacterial QS
response and preventing them from expressing phenotypes controlled by this system
such as biofilm formation or virulence (Case et al. 2011; Harder et al. 2012; Gardiner
et al. 2015). Signals for activation of these defences can be components of the alga
themselves. When the degradation products of one of the main components of the
algal cell wall, agar, is detected, the macro red algae Gracilaria conferta responds
with oxidative bursts and halogenating activity against any potentially pathogenic
bacteria (Weinberger et al. 1999). Interestingly, one of the causative agents of bleaching disease in Delisea, Ruegeria sp. R11, requires glutathione peroxidase to be virulent: presumably this enzyme negates the algal defence mechanism of oxidative
bursts (Gardiner et al. 2015). This pathogen was isolated from D. pulchra; however,
it has a wider host range as it is able to kill two of the three unicellular cell types of
E. huxleyi through the same mechanism of bleaching at elevated temperatures
(Mayers et al. 2016). Microalgae such as the chlorophyte Chlorella saccharophila
have also been found to disrupt QS gene expression in bacteria as well (Natrah et al.
2011), indicating that a similar role may be present in microalgae.
Previous research has proposed that the roseobacter Phaeobacter gallaeciensis
displays a fascinating switch from mutualism to pathogenicity in response to algal
14 Bioactive Small Molecules Mediate Microalgal-Bacterial Interactions
Pseudoalteromonas piscicida was found to be a potent algicidal molecule causing
the death of E. huxleyi (Harvey et al. 2016). The bacterium Alteromonas sp. was
isolated from a harmful algal bloom, and four compounds (2-undecen-1′-yl-4quinolone, 2-undecyl-4-quinolone, 3-hexyl-6-pentyl-4-hydroxyl-2H-pyran-2-one
and 6-heptyl-3-hexyl-4-hydroxyl-2H-pyran-2-one) were isolated which had specific activity against harmful dinoflagellates but had a lower activity against other
microalgae (Cho 2012). Two algicidal compounds, prolyl-methionine and hypoxanthine, were identified from a bacterium Bacillus sp. which was isolated from a
bloom of the haptophyte Phaeocystis globosa; they were found to target antioxidant
systems within the alga (Yang et al. 2015). Lactones produced by Ruegeria pomeroyi were found to target and harm only the algae (Chlorella fusca) when tested
against other bacteria, fungi and the alga (Riclea et al. 2012). In addition to algicidal
molecules, bacteria can also produce molecules that negatively affect the behaviour
of algae. Anatoxin-a and microcystin-LR are two toxins produced by cyanobacteria
that can inhibit motility in the chlorophyte Chlamydomonas reinhardtii and cause
increased settling and sinking of the alga (Kearns and Hunter 2001).
Algae have developed a suite of small molecules that can act as chemical
defences, which they can deploy to inhibit colonization, organisms competing for
available resources or predators (Hay 1996; Wolfe et al. 1997; Potin et al. 2002;
Steinberg and de Nys 2002). For example, (macro) brown algae produce phlorotannins which are potent antimicrobial metabolites against a range of bacteria, fungi
and other algae (Eom et al. 2012). Likewise, microalgae have been shown to produce antibiotic compounds. Various diatoms produce polyunsaturated aldehydes
(PUA) which can inhibit various bacteria (conversely, it was also found to stimulate
a few specific species of bacteria as well) (Ribalet et al. 2008).
One of the most studied chemical defence systems has been in the (macro) red
algae Delisea pulchra, which is subject to bleaching due to various bacterial pathogens (Case et al. 2011; Kumar et al. 2016). The macroalga can release furanones,
similar in structure to the QS AHL molecules, thereby inhibiting the bacterial QS
response and preventing them from expressing phenotypes controlled by this system
such as biofilm formation or virulence (Case et al. 2011; Harder et al. 2012; Gardiner
et al. 2015). Signals for activation of these defences can be components of the alga
themselves. When the degradation products of one of the main components of the
algal cell wall, agar, is detected, the macro red algae Gracilaria conferta responds
with oxidative bursts and halogenating activity against any potentially pathogenic
bacteria (Weinberger et al. 1999). Interestingly, one of the causative agents of bleaching disease in Delisea, Ruegeria sp. R11, requires glutathione peroxidase to be virulent: presumably this enzyme negates the algal defence mechanism of oxidative
bursts (Gardiner et al. 2015). This pathogen was isolated from D. pulchra; however,
it has a wider host range as it is able to kill two of the three unicellular cell types of
E. huxleyi through the same mechanism of bleaching at elevated temperatures
(Mayers et al. 2016). Microalgae such as the chlorophyte Chlorella saccharophila
have also been found to disrupt QS gene expression in bacteria as well (Natrah et al.
2011), indicating that a similar role may be present in microalgae.
Previous research has proposed that the roseobacter Phaeobacter gallaeciensis
displays a fascinating switch from mutualism to pathogenicity in response to algal
14 Bioactive Small Molecules Mediate Microalgal-Bacterial Interactions