Cells of a dinoflagellate reveal reddish areas signifying natural
chlorophyll fluorescence, blue areas indicating DNA and green "dots" marking
the cells of RCA cluster, bacteria implicated as a red tide killer.
Revealing A Killer's Identity
Red tide discovery sheds new light on the role of bacteria in outbreaks
Xavier Mayali extracted hundreds of water samples off the
Scripps Pier in six years as a Scripps Institution of Oceanography at UC San Diego
graduate student, but what he found in summer 2005 was different.
It was then that Mayali found a killer in the water.
With samples of a red tide bloom that occurred in 2005, Mayali and his
advisors, Scripps Professors Peter Franks and Farooq Azam, were able to
uncover new details about algal bloom processes.
Mayali devised highly delicate "micromanipulation" processes involving
washing and testing individual cells of a dinoflagellate, single-celled
plankton, known by the species name Lingulodinium polyedrum. The techniques
revealed that a bacteria, called Roseobacter-Clade Affiliated ("RCA
cluster"), attacked dinoflagellates by attaching directly to the plankton's
cells, slowing their swimming speed, and eventually killing them. Mayali
observed that RCA bacteria attacked dinoflagellates often two or more at
a time.
The research study, which was coauthored by Franks
and Azam, is published in the May 1 edition of the journal Applied
and Environmental Microbiology.
Now a postdoctoral researcher at Scripps, Mayali first became interested
in phycology, the study of algae, as an undergraduate at UC Berkeley. He
decided to pursue a career in science after spending time in the tropics at
Berkeley's Gump Research Station on the island of Moorea in French Polynesia.
By the time he began studying at Scripps, Mayali decided to focus on red tides, also
referred to as harmful algal blooms. Red tides and related phenomena in
which microscopic algae accumulate rapidly in dense concentrations have been
on the rise in recent years, causing hundreds of millions of dollars in
worldwide losses to fisheries and beach tourism activities. While not all
algal outbreaks are harmful, some blooms carry toxins that have been known
to threaten marine ecosystems and even kill marine mammals, fish, and birds.
"My interest in blooms starts from the idea that we really don't
understand why they start and stop, yet they have been doing so since before
humans were around," said Mayali. "Also, we do not know if pollution or
climate change are impacting bloom occurrences. We can put men on the moon,
explore the depths of the ocean 10 kilometers (32,800 feet) down, and
sequence our genome, but we cannot understand an apparently simple issue of
when and how long a single celled phytoplankton will grow to huge numbers.
I just find it a fascinating problem."
Franks said he found it a bizarre concept of scale that Lingulodinium dinoflagellates, which at 25 to 30 microns in diameter are known to swim
through the ocean with long appendages known as flagella, are attacked by
bacteria that are about one micron in size and can't swim.
"It's somewhat shocking to think of something like three chipmunks attaching
themselves to an elephant and taking it down," said Franks.
Another result emerged from the study after Mayali used DNA evidence to
evaluate the prevalence of the RCA bacterium in the oceans. He found
evidence of RCA bacteria in temperate and polar waters around the world,
including in records of algal bloom outbreaks.
"It's possible that bacteria of this type play an important role in
terminating algal blooms and regulating algal bloom dynamics in temperate
marine waters all over the world," said Mayali.
Dinoflagellate interactions with highly abundant and genetically diverse
bacteria in the sea have the potential to both enhance and suppress bloom
intensity�but this important subject is only beginning to be explored.
"The newly identified role of RCA cluster is a good illustration of the need
to understand the multifarious mechanisms by which microbes influence the
functioning of the marine ecosystems," Azam said.
—Mario C. Aguilera
June 2008
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