Chapter 11 Dynamics of Seagrasses
277
understood, and the causes of shoot mortality have
not been elucidated as yet. Shoot mortality is a necessary component of the maintenance of stable seagrass meadows, so that the presence of a stress factor
need not be invoked to account for shoot mortality. These thoughts suggest that, to some extent,
shoot mortality should be considered a component of
clonal integration, such that a clone may selectively
‘decide’ to cease the activity of a particular leafproducing meristem, thereby causing shoot death.
Whereas the activation of seagrass meristems in response to disturbance, such as increased branching
rates (i.e. shoot production) in response to clipping
of apical rhizome meristems (Terrados et al., 1997),
have been examined, the internal controls on loss
of meristematic activity have not been addressed, as
yet. More importantly, there is a need to examine
what factors may cause the death of apical meristems, which would reduce shoot recruitment. The
understanding and capacity to predict meristematic
activity may provide the capacity to detect stress and
forecast mortality before this is reflected in shoot
density changes.
Hence, most knowledge on the controls on shoot
mortality derives from examination of stress and
disturbance factors. Reduced water and sediment
quality leads to shoot mortality, often resulting in
catastrophic seagrass loss through multiple factors.
Deterioration of water quality leads to seagrass mortality through light limitation and unbalanced plant
carbon budgets (e.g. Gordon et al., 1994; Ruiz and
Romero, 2001). Shoot mortality as a consequence
of reduced light penetration has been reported at
the depth limit of seagrass meadows (Krause-Jensen
et al., 2000), and confirmed by shading experiments
(Gordon et al., 1994; Ru´ ız and Romero, 2001). Increased nutrient inputs have also been shown to be
associated to high mortality rates (P´ erez et al., 1994).
Deterioration of sediment conditions, such as increased sediment anoxia and sulfide production has
been shown to lead to seagrass mortality, although
the responses vary greatly across species (Terrados
et al., 1999). Water column hypoxia, also derived
from excessive organic inputs, has also been identified as a factor affecting the health of leaf-bearing
meristems, eventually causing shoot death (Greve
et al., 2003). Sediment disturbance, such as excessive burial and sediment erosion, also causes shoot
death by killing meristems, altering clonal integration, and, when extreme, creating topographical barriers (Marb` a and Duarte, 1994, 1995; Duarte et al.,
1997a). Physical disturbance is also an important
source of shoot mortality, through uprooting of the
plants during storms or due to human activities such
as anchoring, dredging, anchor damage, and trawling (Duarte, 2002). Biological disturbance may also
generate substantial seagrass mortality (e.g. Orth,
1975).
C. Shoot Demography
It is possible to estimate the age of individual shoots
of most seagrass species because there is a relatively
constant rate of production of new leaves on a shoot,
called the plastochron interval. Each leaf leaves a
distinctive scar on the short shoot at the node, so it
is possible to count the number of leaves produced
over the lifespan of an excavated shoot and multiply this number of leaves by the plastochron interval
to estimate the age of the shoot (Patriquin, 1973;
Duarte et al., 1994). Once recruited into the population, shoots of different species have different average lifespans. Shoots of the small, fast-spreading
species, like Halophila spp., have an average lifespan of only a month or so, and a maximum age of
a few months (Table 1). In contrast, the shoots of
the larger, slower-spreading species like Posidonia
spp. and Thalassia spp. have average life expectancies of a few years, with some shoots surviving for
decades. A genetically individual plant may be much
older than individual short shoots, since most seagrasses exhibit monopodial or sympodial growth. As
a rhizome grows through the soil and produces new
shoots, each successive shoot is necessarily younger
than the previous shoots. Older shoots may eventually senesce, but their progeny shoots may continue
to thrive and extend away from the point where a
seedling originally produced the genetically individual plant. Theoretically, genetic individuals could be
as old as the origin of the species, even though individual shoots can only survive a few decades at
most.
Seagrasses, as angiosperms, are all capable of sexual reproduction through flowering and seed production (although sexual structures have not been
observed for all species, e.g. Jewett-Smith et al.,
1997). As long as seeds result from the fertilization
of an ovule by pollen from another genetically distinct individual, the plant originating from that seed
is genetically distinct from others in the population.
Once a seedling becomes established in a seagrass
meadow, it begins to grow up by the production of
277
understood, and the causes of shoot mortality have
not been elucidated as yet. Shoot mortality is a necessary component of the maintenance of stable seagrass meadows, so that the presence of a stress factor
need not be invoked to account for shoot mortality. These thoughts suggest that, to some extent,
shoot mortality should be considered a component of
clonal integration, such that a clone may selectively
‘decide’ to cease the activity of a particular leafproducing meristem, thereby causing shoot death.
Whereas the activation of seagrass meristems in response to disturbance, such as increased branching
rates (i.e. shoot production) in response to clipping
of apical rhizome meristems (Terrados et al., 1997),
have been examined, the internal controls on loss
of meristematic activity have not been addressed, as
yet. More importantly, there is a need to examine
what factors may cause the death of apical meristems, which would reduce shoot recruitment. The
understanding and capacity to predict meristematic
activity may provide the capacity to detect stress and
forecast mortality before this is reflected in shoot
density changes.
Hence, most knowledge on the controls on shoot
mortality derives from examination of stress and
disturbance factors. Reduced water and sediment
quality leads to shoot mortality, often resulting in
catastrophic seagrass loss through multiple factors.
Deterioration of water quality leads to seagrass mortality through light limitation and unbalanced plant
carbon budgets (e.g. Gordon et al., 1994; Ruiz and
Romero, 2001). Shoot mortality as a consequence
of reduced light penetration has been reported at
the depth limit of seagrass meadows (Krause-Jensen
et al., 2000), and confirmed by shading experiments
(Gordon et al., 1994; Ru´ ız and Romero, 2001). Increased nutrient inputs have also been shown to be
associated to high mortality rates (P´ erez et al., 1994).
Deterioration of sediment conditions, such as increased sediment anoxia and sulfide production has
been shown to lead to seagrass mortality, although
the responses vary greatly across species (Terrados
et al., 1999). Water column hypoxia, also derived
from excessive organic inputs, has also been identified as a factor affecting the health of leaf-bearing
meristems, eventually causing shoot death (Greve
et al., 2003). Sediment disturbance, such as excessive burial and sediment erosion, also causes shoot
death by killing meristems, altering clonal integration, and, when extreme, creating topographical barriers (Marb` a and Duarte, 1994, 1995; Duarte et al.,
1997a). Physical disturbance is also an important
source of shoot mortality, through uprooting of the
plants during storms or due to human activities such
as anchoring, dredging, anchor damage, and trawling (Duarte, 2002). Biological disturbance may also
generate substantial seagrass mortality (e.g. Orth,
1975).
C. Shoot Demography
It is possible to estimate the age of individual shoots
of most seagrass species because there is a relatively
constant rate of production of new leaves on a shoot,
called the plastochron interval. Each leaf leaves a
distinctive scar on the short shoot at the node, so it
is possible to count the number of leaves produced
over the lifespan of an excavated shoot and multiply this number of leaves by the plastochron interval
to estimate the age of the shoot (Patriquin, 1973;
Duarte et al., 1994). Once recruited into the population, shoots of different species have different average lifespans. Shoots of the small, fast-spreading
species, like Halophila spp., have an average lifespan of only a month or so, and a maximum age of
a few months (Table 1). In contrast, the shoots of
the larger, slower-spreading species like Posidonia
spp. and Thalassia spp. have average life expectancies of a few years, with some shoots surviving for
decades. A genetically individual plant may be much
older than individual short shoots, since most seagrasses exhibit monopodial or sympodial growth. As
a rhizome grows through the soil and produces new
shoots, each successive shoot is necessarily younger
than the previous shoots. Older shoots may eventually senesce, but their progeny shoots may continue
to thrive and extend away from the point where a
seedling originally produced the genetically individual plant. Theoretically, genetic individuals could be
as old as the origin of the species, even though individual shoots can only survive a few decades at
most.
Seagrasses, as angiosperms, are all capable of sexual reproduction through flowering and seed production (although sexual structures have not been
observed for all species, e.g. Jewett-Smith et al.,
1997). As long as seeds result from the fertilization
of an ovule by pollen from another genetically distinct individual, the plant originating from that seed
is genetically distinct from others in the population.
Once a seedling becomes established in a seagrass
meadow, it begins to grow up by the production of