COMPETITION, PREDATION, PARASITISM,
SYMBIOSIS,
ETC.
LINKS & References
Competition notes
Textbook chapter 6, pp. 188-201 for Monday,
rest of chapter for Wednesday.
- The equation... p. 198 &
http://www.blackwellpublishing.com/townsend/model/model05.html
#6 &7 :
know what all the terms mean and what will cause left side of equation to rise and fall
-
Competitive exclusion law
math (isoclines and others) shows coexistence is impossible
unless.... be able to finish the "unless"
- Research types....
- Good: documenting the mechanism of competition or the resource
(=niche axis) involved
fig 6.2 a and b
and fig. 6.6
- better: Showing that the realized niche axis is smaller than
the fundamental niche axis
fig. 6.4
- best: showing that the competition affects The
Equation or at least some component of it
fig 6.2 c and
fig 6.3
- Know the details of the classic experiments--
Gause's Parameciums
barnacles
barnacles
alsoo
diatoms
fig. 6.1 and fig. 6.5
(Darwin`s finches when we come back to chapter 2)
- Be able to analyze any other experiment... fig.
6.9,
6.10,
6.13,
6.14 &
6.15,
6.16,
6.17,
6.18 etc.
Was the hypothesis aimed at good -better- or best?
- Questions (p. 222) #1, 2, 3, 4, 5, 6 (see fig.6.9 ,
6.15), 8 (see fig.6.13 ,
6.14), 9 (6.16)
- Bigger questions for after the midterm but under discussion Wednesday, basically the
role of competition in evolution (niche selection) and in community structure-- is
competition more important than mutualism and predation? Are
realized niches ever bigger than fundamental niches (http://www.sciencemag.org/cgi/content/full/299/5607/644)?
- ghost of competition past (question #7 on p.
222, fig 6.12,
6.13)
- paradox of the plankton
6.14
- "the world is green" hypothesis vs. "the world is prickly
and tastes funny"
fig. 1.8
- fair-weather ecology and the lessons of Hurricane Hugo
- neutral model (question #10 on p. 222)
SYMBIOSIS & MUTUALISM NOTES
(including PARASITES, Part I (PART II is later): Textbook
Chapter 7
Wednesday: Pages 222-240 Questions p. 254 :
#1, 2, 3, 4, 5 (fig 7.19)
FOR
FRIDAY
Finish this chapter and be able to answer #6, 7, 8, 9, 10.
THEORETICAL CONSIDERATIONS:
- One part of this assignment is how hosts respond
to internal symbionts. Some biologists believe that a true parasite ALWAYS changes
the behavior or anatomy or physiology of the host in such a way as to favor the fitness of
the parasite. Notice for parasites, fitness is not necessarily
just survival and reproduction-- it's survival, reproduction,
and transmission or dispersal to the next host. Look at the examples in the book (threadworms
which are like American pinworms,
fig. 7.12), and the
Wolbachia example below and maybe even this: http://www.salon.com/health/books/2000/09/26/parasite/index.html
and be prepared to discuss this point.
- so if parasites always change their habitats so as
to improve parasite descendent fitness.... do other critters also change their habitats to
enhance their "fitness"???? Or are parasites the only ones?
- Some ecologists think that, in habitats which have
been stable for a long time [so that the presence of both species becomes predictable to
each other], coevolution tends to follow this sequence:
parasitism --> commensalism --->
facultative mutualism or symbiosis ---> obligatory mutualism or symbiosis.
- Also there's been a lot of research lately on the
evolving loss of pathogenicity in diseases.
- fig. 7.18:
is it virulence or transmissibility which evolves? why?
- Evolution and the Origins of Disease (relatively easy technical
article from Scientific American magazine; has good links to more
information): http://www.sciam.com/1998/1198issue/1198nesse.html
- "The history of evolution and biodiversity is fundamentally a history of the
evolution of species interactions." "Most living organisms have evolved
in ways that absolutely require them to use a combination of their own genetic machinery
and that of one or more other species if they are to survive and reproduce."
"Even now, among human populations one-third of deaths are caused by infectious
disease." "As we continue to manipulate biodiversity, our experience so
far with the evolution of virulence in diseases, short-term effectiveness of resistant
crop varieties, and rapid evolution of interactions within natural communities suggests
that the health and welfare of human societies will demand an increased understanding of
the ongoing evolutionary dynamics of species interactions." excerpts from http://www.sciencemag.org/cgi/content/full/284/5423/2116
-
applications #1:
http://www.sfgate.com/cgi-bin/article.cgi?file=/news/archive/2003/02/10/state1537EST0084.DTL
aliens have fewer parasites
- And increasing interest in the ecology of infectious disease in
general:
-
Society for Vector Ecology studies all aspects of the biology,
ecology, and control of arthropod vectors and the
interrelationships between the vectors and the disease agents
they transmit. http://www.sove.org
-
Date sent: Wed,
28 Feb 2001 17:41:04 -0500
From: SSCHEINE <sscheine@NSF.GOV>
Organization: National
Science Foundation
Subject: RFA:
Ecology of Infectious Diseases
To: ECOLOG-L@UMDD.UMD.EDU
Request for Applications: Ecology of Infectious
Diseases
The National Institutes of Health (NIH), the
National Science Foundation (NSF) and the U.S. Geological Survey
(USGS) invite applications for the establishment of research
programs to elucidate the underlying mechanisms that govern the
relationships between anthropogenic environmental changes and
the transmission dynamics of infectious diseases.
This Request for Applications (RFA) calls for
the development of interdisciplinary research programs on the
ecology of infectious diseases in the context of anthropogenic
environmental changes such as biodiversity loss, habitat
transformation, environmental contamination, climate
change and other influences. The focus of this RFA is on
discovery of basic ecological and biological mechanisms and
development of predictive models for the emergence and
transmission of diseases in humans and other animals, and
ultimately the development of strategies to prevent or control
them. This is the second RFA issued for this program.
The most significant change from the previous RFA is a more
inclusive definition of relevant climate
change-disease projects.
The complete RFA can be found at :http://grants.nih.gov/grants/guide/rfa-files/RFA-TW-01-004.html
-
another case study: "Because males cannot pass the bacteria on in sperm,
Wolbachia
have evolved many sophisticated strategies to skew populations in
favor of infected females (Science, 11 May 2001, p. 1093).
Out of sync. Parasitic bacteria delay a key
chromosomal movement in Nasonia wasps." On page 1124
of this issue, researchers at the University of California, Santa
Cruz, offer the first good glimpse of how Wolbachia do this
in a species of wasp known as Nasonia vitripennis. In these
wasps, as in many insects, the sex of the offspring is normally
determined by a bizarre process: If an egg is fertilized by a sperm,
the progeny will be female, but unfertilized eggs will divide and
develop into male embryos. Wolbachia play havoc with Nasonia's
reproduction. When an infected male mates with a healthy female, the
offspring will all be male, but if two infected wasps mate, the
result will be a normal ratio of male and female offspring, all
infected with the bacterium.
"Skewing the sex ratio in this way works to Wolbachia's
evolutionary advantage. By making uninfected female wasps produce
only sons, the bacteria reduce the number of uninfected female wasps
in the population. That makes it more likely that Wolbachia
from other females will get carried down from one generation to the
next.
"Researchers have been unable to expose how Wolbachia
perform such manipulations largely because they haven't had the
right tools, according to co-author William Sullivan. "You
couldn't answer these questions 5 years ago," he says.
"The technology just wasn't there." In recent years,
however, Sullivan and others have figured out how to create movies
of a developing embryo that reveal the activity of its proteins and
genes. N. vitripennis's eggs develop slowly, making them
ideal for a starring role.
"Once the wasp's egg is fertilized, its chromosomes go through a
complex choreography. The compartments that contain each set of
chromosomes (called the pronuclear envelopes) move to a special
location in the egg known as the metaphase plate, then the envelopes
break down, allowing the chromosomes to escape and find their
correct place at the plate. Only then can they be duplicated as the
egg divides into new cells.
"Sullivan and postdoc Uyen Tram observed this process using dyes
that attach to proteins that help destroy the walls of the male and
female pronuclei. They found that Wolbachia tinker with the
timing mechanism. In healthy wasps, both pronuclear envelopes were
destroyed at the same time. But when the sperm came from an infected
male, its pronuclear envelope started decaying a minute or more
after the uninfected female's, preventing the enclosed chromosomes
from arranging appropriately before the cell divided. The egg then
divided as if it had never been fertilized, using only the
chromosomes from the mother to develop into a male.
"Because Wolbachia block an infected male's chromosomes
with a simple change of timing, they can bring the process into sync
with an equally simple trick. When Tram and Sullivan fertilized an
infected egg with sperm from an infected male, the walls of the
female's pronuclear envelope also took longer to disintegrate. As a
result, both parents' chromosomes were released late, so that both
became part of the embryo's genome. Such infected wasps, in turn,
grow up to do their bacterial puppet masters' reproductive
bidding."
http://www.sciencemag.org/cgi/content/full/296/5570/999a
-
More and more ecologists doubt that pure
commensalism ever exists. When we closely study cases of apparent commensalism, we nearly
always discover some kind of benefit to the host. For example, when intestinal commensals
are removed with antibiotics, they are commonly replaced by intestinal parasites; thus the
"commensals" were at least out-competing populations which would harm the host,
and in many cases the "commensals" can be shown to be providing the host with
vitamins or ethanol. For example, "Molecular Analysis of Commensal Host-Microbial Relationships in the Intestine"
http://www.sciencemag.org/cgi/content/full/291/5505/881
- Rathke has suggested that mutualism has been a
greater force in evolution than has competition. Most of her work is in pollination
mutualism. Your instructor has not found a groundswell of biologists leaping on this
bandwagon, but actually research in mutualism is relatively uncommon anyway, even in
pollination and deep sea frontiers. Rathke says that if Darwin had lived at another
time and place and had been another sex (and not a male in England during the Adam Smith
world view of free enterprise and imperialism), our view of the "struggle for
existence" could have been more like the "search for
compatibility." or maybe
congeniality?
CONSUMERS & THEIR VICTIMS
1. Introduction (For Monday: Read pp.
259-275; p. 294 #1, 2, 3, 4, 5,)
DEFINITIONS.
- A PREDATOR (generic) eats another organism, the PREY.
- A TRUE PREDATOR kills an individual prey organism and then eats at
least part of it; the predator kills many prey victims in its lifetime. Examples: cats,
dogs, falcons, seed-eating birds and rodents, Venus fly-traps, slime molds, humans.
- A GRAZER eats only parts of many different victims. Ex: Bambi,
Thumper, slugs, and (according to some) transient ectoparasites like blood-sucking insects
and worms.
- A PARASITE eats only part of one or a few HOST victims;see above
- A HERBIVORE is any of the above if the victim is a plant.
TYPES OF EXPERIMENTS (discussed in more
detail below)
- measuring effects on population sizes, fecundity, growth rates ,etc.
(hardly ever niche stuff although fig. 8.2 comes close, but hypothetically.you
could....) fig. 8.1,
8.3,
8.4,
8.8
- measuring the changes in consumer responses to changes
in victim density. For example, a filter feeder just loses
effectiveness, but other predators may change strategies-- switching
to less desirable prey, migrating to new patches, transmission to new
hosts, foraging over greater range, etc. A major activity among
current experimenters is the testing of models about
theoretically ideal consumer behavior [like optimal or marginal diets
and optimal foraging].
- measuring the changes in victim responses to changes in consumer density or
attack. For example, changes in life histories and reproductive allocations
(compensation) or in host
behavior or physiology or chemistry.
- documenting mechanisms by which victims try to avoid consumers; for
example, camouflage, flocking, chemical defenses, periodicity, genetic variability, etc.
[mostly oh my science, but increasingly actually doing experiments these days]
- [often overlaps with any of the above] documenting genetic changes resulting from
selective forces of the consumer game.
Theoretical basis for many contemporary studies =
COST/BENEFIT ANALYSIS and GAME THEORY. Ideally, the ecologist estimates the costs
(energy expenditures [ante] & risks) and the benefits (potential energy gain [stakes]
& probability of winning) for various behaviors and mechanisms to predict what
specific populations should do; then the ecologist tries to see whether real populations
fit the theoretical strategy models.
Remember that a "strategy" must evolve; an individual or
population with a particular behavior must be more fit than its competitors--it must both
survive and leave more copies of its genes; it must "win" more often than it
loses; it must maximize its predator's costs while minimizing its own costs and risks.
Remember that winning at any cost [energy] will severely reduce reproductive resources,
leading to losses in the evolutionary game. [Cost/benefit analysis is also used in other
areas of ecology, such as in competition theory and dispersal theory. And we'll come
back to evolution in the next chapter we study.
And remember that you want to compile ideas about what
strategies your critter has.]
2. Victim Defenses, pp 264-9; p. 294 #2, 3,
4 (still part of Monday's assignment)
Compensation (allocation changes): fig.
8.5,
8.7
The textbook concentrates on victims who are plants, but in addition, here
is an outline of another view of prey defenses. Evolutionarily
feasible prey responses to changing predator numbers are nearly always genetically
pre-programmed because predators are always predictably present; predators are strong
selective forces. The game-theory "strategies" which an ecologist would predict
would be to maximize the predator's cost and minimize the predator's benefits while
minimizing the prey's costs and risks. Some examples of prey strategies:
1. Escape by time (synchronous behavior) and or
prey number (aggregation or patchiness) like flocking and then migrating or
hibernating before predator population can increase or, even better, by being periodical
in prime number years like cicadas. (Note that these "strategies" work only when
the patches or flocks are rare in time or space.) These responses increase
predator's search time, decrease his benefits, and minimize the risks to the prey
individual who escapes while the predator is handling another prey individual. The
predator may even starve to death before he finds the patch or flock.
3. Escape by size [increase predator's handling losses and handling
time (time = money = energy)]: be too big like a coconut or elephant, too tall like a
vine, too small like begonia seeds.
4. Invest in
- chemical defenses and poisons to reduce predator benefits and increase his risks
(skunks), which is what the textbook emphasizes; also see some recent research
reported in Science about trees which change an array of nasty
chemicals throughout the growing season so that consumers will have a really hard time
evolving antidotes to everything.
fig 8.6
- or cheaper camouflage to increase predator's search time, or
- aposematism [=warning "labels"] if you or your mimicry model also have
a chemical defense and if your predators learn [unlike most dogs who have
encountered skunks]. or just have ....
- Strategies for recovery, planning on sacrificing to predators and other consumers,
generally what the book calls compensation.
3. CONSUMER BEHAVIOR,
Foraging, etc. pp. 268-275, p. 294 #5 (still
part of Monday's assignment)
[1] NET energy (calorie) gain [= energy value of the
food minus the energy lost waiting, searching, chasing, killing, butchering, digesting,
losing to competitors and decomposers, etc.]
[2] other nutritional values of the food [beyond calories--protein,
minerals, vitamins, etc.]
[3] dilution and neutralization of toxins in other foods
[4] avoidance of the risk of becoming prey for another predator
species.
[5] What if the consumer is a parasite or a
symbiont?
How should consumer populations behave when
victims become either common or rare? (What are some evolutionarily feasible
predator responses to changes in prey density?)
[1] Change density of consumer population rapidly
to adjust by migration or reproduction or cannibalism or other life-history traits.
[2] Change behavior, like
[a] Foraging Behavior. For prey with aggregated dispersion (patches),
the predator must "decide" when to leave one patch to search for another. The
basic idea is that the predator should leave before the benefits of staying and consuming
more energy are outweighed by the costs of finding and handling the prey within the patch
plus the costs of finding the patch in the first place. Predators generally seem to have
evolved foraging behavior which reasonably matches optimal cost/benefit ratios, especially
when you take into consideration the complications of non-feeding behaviors and risks
associated with dispersal. For example, most predators and parasites are prey and/or hosts
for other populations. Thus the prey-seeking costs for a predator include the increased
risks of being eaten while foraging. fig.
8.10
[b] Other behavioral responses to low victim density include
minimizing costs by sleeping or hibernating to save energy or switching to less
desirable but cheaper or at least more available prey species.
fig. 8.12
4. (Wednesday) Consumer/Victim
Population Details: 276-289, #6, 9
http://www.blackwellpublishing.com/townsend/model/model08.html
Other ways to see the EXPONENTIAL
GROWTH EQUATIONS
N1 = V = prey, host, victim, etc.
population size
N2 = C = predator, consumer etc. population size
ß = impact each unit of the second population has on the first
population
dV/dt = rV - ßC [the
exponential growth curve of the prey population is modified when predators eat them; the
modification is proportional to the size of the predator population.]
dC/dt = rC
= rbirthrateC - rmortalityrateC
[the exponential growth curve of the predator population can be
expressed as its birth rate minus its death rate, but....]
dC/dt = ßV - rmortalityrateC
[but since the consumer birth rate is equivalent to
the amount of energy it accumulates by eating the prey, ßV....]
Can you express any equations in box
8.2, in these terms?
CYCLES for simple (2 population) predator/prey situations
look like superimposed waves (the classic lynx/hare data
fig. 8.17 taken from the
fur-buying records of the historical Hudson Bay Company) because as the prey population
increases, the predator population can eat more; so the predator population grows, but
this consumption causes the prey population to decline; so then there is less for the
predator population to eat and the predator population declines; then
because of less predation, the prey population increases and the predator population can
eat more; so the predator population grows, but this consumption causes the prey
population to decline; so then there is less for the predator population to eat and the
predator population declines; then because of less predation, the
prey population increases and the predator population can eat more; so the predator
population grows, but this consumption causes the prey population to decline; so then
there is less for the predator population to eat and the predator population declines;
then because of less predation....
Can you figure out how these same equations help explain
fig 8.22 and
fig. 8.18?
("no" is not the right answer)
REGULATED GROWTH EQUATIONS are
sometimes better models for predator/prey situations in complex
communities [note similarity to competition equations] also see
fig 8.19
PREY: dN1/dt = r1N1 (K1
- N1 - ßN2) / K
OR dV/dt = rV (Kv - V - ßC) /
Kv
PREDATOR: dN2/dt = r2N2 (K2
- N2 + ßN1) / (K2 + ßN1
OR dC/dt = rC (Kc
- C + ßV) / (Kc + ßV)
[assuming that food V is smallest niche axis]
The logistic equations sometimes work for an over-all
metapopulation (pp. 286 ff.) even when the patchy sub-populations are doing exponential,
cyclical predator/prey games.
5. (Friday) Other considerations. pp.290-294; p. #10 and recap.
Review
http://www.blackwellpublishing.com/townsend/model/model10.html
keystone predators, biodiversity, etc.
A note about genetic basis of behavior changes: If the
change in prey density is predictable [like seasonal, for example], then a
genetically-programmed predator or parasite behavioral change [e.g., instinct] would be a
good idea. Many predators [even bacteria] travel farther or move to new
"patches" more quickly when food is in low concentration. However, the
evolution of more complex behaviors is fairly rare because of all the
anatomical/physiological components which are involved. Moreover, these components are
expensive. If the change in prey density is mostly unpredictable, then a learned behavior
is cheaper, but.... what risks are involved and what probabilities change?
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