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Please read
the short abstract below>
Fisheries
in US & Canada: Is overfishing or habitat destruction the key culprit
in fishery depletion along the east coast?
How big
a problem?
US
40% of fish stocks are over exploited
Grand
Banks/New Foundland which has been fished for 350+ years : fisheries
have been closed in 7 out of 8 of cod stock areas. 40,000 fishermen
forced to abandon their traditional livelihood
Catch
declines in these areas: 87' 452,00 cubic tons ---> 93' 81,000 cubic
tons ---> 94' 22,000 cubic tons
Why?
1. Over
fishing models predicted early on that large catches would threaten populations
but managers who awarded permits and regulations wanted to maintain relationship
with fishermen. This resulted in 60% actual removal of adults over the
20% recommended by modelers.
2. Predation
by seals which were increasing in number with protection
3. Cold
seawater changes due to climatic changes whether human or naturally induced
4. Reduction
in forage fish for cod.
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5. Poor production of young
cod to replace declining adults: research indicated that age of
sexual maturity dropped in cod from 6-7 year to 2.78-5.08 years
dependent on site sampled. Smaller younger fish produce less eggs
( 370 K relative 1.6 million eggs a older, larger cod can produce).
The eggs themselves are smaller reducing the probability of survival,
combined with less eggs results in less offspring making it to juvenile
stages. Also, fewer spawning periods were noted.
From text should reflect
that this is a perfect example of compensatory response: as
population lost adults, younger individuals who could reproduce
were selected since they are they only ones who could contribute
thief genes to the next generation. This contains a genetic selection
connotation - we have selected for r -types in a species which was
previously more K-type. I suppose the good news was the species
was "genetically plastic or variable to make this transition.
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The materials below are taken from: http://www.ultranet.com/~jkimball/BiologyPages/T/Telomeres.html
* Telomere functions
Telomeres
Each eukaryotic chromosome consists of a single molecule of DNA associated
with a variety of proteins.
Example: an average human chromosome contains a single molecule of DNA
of about 150 million nucleotide pairs (150 x 106 bp). Stretched to its
full length, this molecule would extend 5 cm. (about 2 inches). In the
chromosome, this molecule is packed into a much more compact structure.
The packing reaches its extreme during mitosis when this chromosome would
condense to a structure some 5 µm long (a 10,000-fold reduction
in length).
The DNA molecules in eukaryotic chromosomes are linear; i.e., have two
ends. (This is in contrast to such bacterial chromosomes as that in E.
coli that is a closed circle, i.e. has no ends.) The DNA molecule of a
typical chromosome contains
* a linear array of genes (encoding proteins and RNAs) interspersed with
* much non-coding DNA.
Included in the non-coding DNA are
* long stretches that make up the centromere and
* long stretches at the ends of the chromosome, the telomeres.
 Telomere functions
Telomeres are crucial to the life of the cell. They
* keep the ends of the various chromosomes in the cell from becoming entangled
and sticking to each other
* they assist in the pairing of homologous chromosomes and crossing over
during prophase of meiosis I.
The telomeres of humans (and mice) consist of as many as 2000 repeats
of the sequence 5' TTAGGG 3'.
5'...TTAGGG TTAGGG TTAGGG TTAGGG TTAGGG TTAGGG..3'
3'...AATCCC AATCCC AATCCC AATCCC AATCCC AATCCC..5'
Replication of linear chromosomes presents a special problem.
DNA polymerase can only synthesize a new strand of DNA as it moves along
the template strand in the 3' -> 5' direction. This works fine for
the 3' -> 5' strand of a chromosome as the DNA polymerase can move
uninterruptedly from an origin of replication until it meets another bubble
of replication or the end of the chromosome. However, synthesis using
the 5' -> 3' strand as the template has to be discontinuous. When the
replication fork opens sufficiently, DNA polymerase can begin to synthesize
a section of complementary strand - called an Okazaki fragment - working
in the opposite direction. Later, DNA ligase stitches the Okazaki fragments
together.
In the figure on the right, the horizontal black arrows show the direction
that the replication forks are moving. Wherever the replication fork of
a strand is moving towards the 3' end, the newly-synthesized DNA (red)
begins as Okazaki fragments (red dashes).
This continues until close to the end of the chromosome. However, the
molecular requirements of the process are such that 5' end of each newly-synthesized
strand cannot be completed. Thus each of the daughter chromosomes will
have a shortened telomere.
It is estimated that human telomeres lose about 100 base pairs from their
telomeric DNA at each mitosis.
This represents about 16 TTAGGG repeats. At this rate, after 125 mitotic
divisions, the telomeres would be completely gone.
Is this why normal somatic cells are limited in the number of mitotic
divisions before they die out?
Telomeres and Cellular Aging
Telomeres are important so their steady shrinking with each mitosis might
impose a finite life span on cells. This, in fact, is the case. Normal
(non-cancerous) cells do not grow indefinitely when placed in culture.
See Cancer Cells in Culture for a discussion of the differences between
normal and cancerous cells grown in culture.
Cells removed from a newborn infant and placed in culture will go on to
divide almost 100 times. Well before the end, however, their rate of mitosis
declines (to less than once every two weeks). Were my cells to be cultured
(I am 67 years old), they would manage only a couple of dozen mitoses
before they ceased dividing and died out.
Could shrinkage of telomeres be a clock that determines the longevity
of a cell lineage?
Evidence:
Some cells are immortal.
* the cells of the germline (the germplasm)
* unicellular eukaryotes (like Paramecium)
* some cancer cells
It turns out that these cells are able to maintain the length of their
telomeres. They do so with the aid of an enzyme telomerase.
Telomerase
Telomerase is an enzyme that adds telomere repeat sequences to the 5'
end of DNA strands. By lengthening the strand prior to replication, cells
with active telomerase are able to compensate for telomere shortening
during DNA replication.
Telomerase:
* is a ribonucleoprotein
* Its single RNA molecule provides an AAUCCC (in mammals) template to
guide the insertion of TTAGGG.
* Thus telomerase is a reverse transcriptase; synthesizing DNA from an
RNA template.
Telomerase is generally found only in
* the cells of the germline, including embryonic stem (ES) cells
* unicellular eukaryotes
* cancer cells
However, when normal somatic cells are transformed in the laboratory with
DNA expressing telomerase, they continue to divide by mitosis long after
their normal life span is over. And they do so without any further shortening
of their telomeres. This remarkable demonstration (reported by Bodnar
et. al. in the 16 January 1998 issue of Science) provides the most compelling
evidence yet that telomerase and maintenance of telomere length are the
key to cell immortality
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Pro:
Cons: