Re: What "New Lyme Spirochete"????
a_weisman_at_yahoo.com
Date: 02/24/05
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Date: 24 Feb 2005 05:20:31 -0800
derdrittemann2003@yahoo.com wrote:
<SNIP>
> Durland Fish, a couple of years ago. It was announced by Yale, and
the
> press release said the borrelia was "97%" similar to B.
Miyamatoi(Sp)?
> a species of borrelia that causes relapsing fever in Japan.
>
> And so, my question, aside from the obvious problems this causes for
> testing and understanding what symptoms come from what...
>
> ...is how does something 97% "similar" windup in ticks in
Connecticut?
I don't think that the 97% similarity should shock you. 3% difference
is enough to make two things VERY different!
See article below:
Evolutionary genetics: All genomes great and small
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v417/n6887/full/417374a_r.html
Nature 417, 374 - 376 (23 May 2002); doi:10.1038/417374a
Evolutionary genetics: All genomes great and small
Chromosome size and number can vary widely between closely related
organisms. This poses a challenge for the evolutionary geneticists who
are trying to make sense of genome structure, says Jonathan Knight.
What's in a number? Genome size and chromosome number seem unrelated to
complexity. The figures above are for haploid genomes - most cells
are diploid (2n), carrying two copies of each chromosome.
We are somewhat like bananas, at least as far as our genes are
concerned. About a third of human genes are clearly related to those
found in plants. Fruitflies, sitting closer to us on the tree of life,
share about two-thirds of our genes. And mice, being fellow mammals,
are at least 90% genetically similar to us.
But look at the size and structure of the chromosomes on which those
genes sit, and the neat correlation between evolutionary relatedness
and genomic similarity breaks down. Sheep have 27 pairs of chromosomes;
the Indian muntjac deer has just 3. We have some 3 billion DNA base
pairs; one species of amoeba has more than 600 billion.
It seems entirely random. But as the genomes of ever more organisms are
sequenced in their entirety, trying to make sense of natural
variability in genome structure has become a burgeoning field. "We're
finally able to ask some key questions," says Daniel Hartl, an
evolutionary geneticist at Harvard University.
Although it is still early days, comparisons of sequences from
different species suggest that events such as bursts of activity of
'jumping genes', genetic duplications and chromosome fusions play a key
role in evolution. Far from being a mass of junk DNA that holds a small
but precious cargo of genes, geneticists are starting to see
chromosomes as highly dynamic stages on which important evolutionary
processes are played out.
Jump to it
The mobile elements known as transposons are among the most powerful
forces that shape chromosome evolution. These 'jumping genes' carry
instructions for their own excision, duplication and insertion into the
genome. It seems that, at certain periods in evolutionary history,
transposon activity made chromosomes expand like accordions. As a
result, most chromosomes are now filled with the silent remnants of
transposons.
Evolutionary geneticists can work out how long ago a transposon became
immobilized by looking at the accumulation of mutations in its
characteristic flanking sequences. Such studies have suggested that a
flurry of transposon activity doubled the size of the maize genome from
1.2 billion to 2.4 billion bases in the past 3 million years1. In human
evolution, transposons called long interspersed elements (LINEs) have
expanded to about 100,000 copies in several bursts over the past 100
million years, the most recent event having occurred 25 million years
ago2. LINEs now account for 15% of human DNA.
Daniel Hartl thinks deletion determines genome size.
Why should mobile elements disperse themselves in bursts? One
intriguing idea, says Hartl, is that most of the time cells repress
transposon activity - a sensible strategy, given that a gene can be
disabled if a transposon jumps into its sequence. But the costs and
benefits may shift during periods of greater evolutionary stress.
Increased rates of transposition might then be selected for, Hartl
argues, because they may help organisms to adapt in tough times by
increasing genetic variability.
Transposons aren't the only type of DNA that can be duplicated. If
there is one thing DNA is good at, it is being copied. And as a result,
duplications ranging from hundreds of bases to the cell's entire
complement of chromosomes have figured heavily in the evolution of
modern genomes.
The simplest duplications produce adjacent repeated sequences that are
all orientated in the same way. The lengths of these 'tandem repeats'
can vary greatly, and often entire genes are duplicated. The extra copy
can then accumulate mutations; often these will render it useless, but
a new and useful function can also emerge. Gene duplication is now
widely considered to be the most likely origin of gene clusters, in
which natural selection has shaped copies of one original gene to take
on different functions. We owe our wide-ranging sense of smell, for
instance, to the duplication and diversification of olfactory-receptor
genes3.
Duplicated DNA need not end up close to its template. The human genome
contains duplicated chunks of DNA hundreds of kilobases long at
opposite ends of a chromosome or on different chromosomes altogether4.
Evan Eichler, a genome researcher at Case Western Reserve University in
Cleveland, Ohio, estimates that at least 5% of the human genome arose
through this sort of duplication5. Indeed, the true figure may be much
higher, as duplications in an ancestor that lived more than 40 million
years ago would by now be undetectable because of the subsequent
divergence of the copied regions.
U. NEUSS
Evan Eichler is looking for new genes in a duplication salad.
Eichler and his colleagues have found that more than a third of
duplicated regions that end up on another chromosome are found near the
centromere, the anchor point for the protein filaments that yank
freshly divided chromosomes apart during cell division. Centromeres
consist mainly of tandem repeats, 171 bases long, known as -satellite
DNA. This DNA tends to remain tightly packed in a structure called
heterochromatin, where it is not transcribed into RNA. But some
centromeres in the human genome have an intermediate region between the
satellite DNA and the adjacent, less closely packed 'euchromatin' that
houses active genes. Eichler's group has found that duplicated segments
may pop up as islands in a sea of -satellite DNA in a region known as
the pericentromere6.
Some pericentromeres are part vacuum cleaner, part blender. They suck
in duplications, chop them up and recombine them. As new insertions
arrive, they drop in without respect for other insertions, sometimes
splitting them in two. Once in a pericentromere, sections of duplicated
DNA are clipped out, inverted and stuck in elsewhere. The result is a
tossed salad of duplications - which Eichler suspects may serve as an
incubator of new genes.
Garbage or gold?
Many of the duplications have brought with them the regulatory
sequences that allow them to be transcribed, and Eichler's team has
detected RNA messages from pericentromeric regions7. Although most of
the resulting transcripts are garbage, there is the possibility that
one could occasionally code for a new and useful protein. So far, no
example of a new gene being born this way has been found. But Eichler
is examining the regions around a 'dead' centromere on human chromosome
2. Here there are higher rates of transcription than around the
chromosome's active centromere, and Eichler hopes to find new and
interesting genes.
Other researchers are studying analogous regions of repetitive DNA that
sit adjacent to the telomeres that cap chromosomes' ends. Like
pericentomeres, these 'subtelomeres' seem to be zones of active genetic
recombination. Researchers led by Barbara Trask of the Fred Hutchinson
Cancer Research Center in Seattle have shown that sections of
subtelomere some 50-100 kilobases long have moved from one chromosome
to another in our species' recent evolutionary history8.
Trask has also found several members of the family of
olfactory-receptor genes hiding in human subtelomeres, at least one of
which seems to be functional, being expressed in the olfactory
epithelium9. Together, her discoveries suggest that, like
pericentromeres, subtelomeres may be important regions for the mixing
and matching of duplicated DNA to form new genes.
Intriguingly, in earlier studies carried out at the Lawrence Livermore
National Laboratory in California, Trask found that most of the
variability in overall genome size across human populations is due to
variation in the sizes of pericentromeres and subtelomeres10. In the
case of chromosome 21, this variation makes the chromosome 45% larger
in some people than in others. The expansion of subtelomeres could be
functionally and evolutionarily significant, Trask suggests.
Doubling up
Such duplication and recombination events cannot explain the wide
variety in chromosome number seen in nature. But individual
chromosomes, and even entire sets, can also be duplicated. More than
three decades ago, Susumu Ohno, a geneticist at the City of Hope Cancer
Center in Los Angeles, proposed that genome duplication could account
for the relatively rapid evolution of complexity in vertebrates11.
Most organisms are diploid - they carry two copies of each
chromosome, one from their father, one from their mother. But an error
in chromosome segregation can easily result in an individual being
tetraploid, carrying twice the usual complement of chromosomes. Ohno
argued that this was a key factor in vertebrate evolutionary history.
Over time, mutations would accumulate in the duplicated chromosomes
until they were so divergent that they were clearly distinct. The
organism would then seem to be diploid once more - only now it would
have twice the number of chromosomes.
Examples of genome duplication are easy enough to find, particularly in
flowering plants, where only about half of all species are diploid.
Wheat, for example, has six copies of each chromosome. And when plant
biologists examined the genome sequence of the diploid thale cress
(Arabidopisis thaliana), they concluded from extensive evidence of
duplication that it must have evolved from a tetraploid ancestor that
first arose around 112 million years ago12.
K. HOKAMP
The yeast genome was shaped by duplication, says Kenneth Wolfe.
Similar polyploidy almost certainly figured in the evolution of the
yeast Saccharomyces cerevisiae, adds Kenneth Wolfe, a geneticist at
Trinity College Dublin. In 1997, he reported that the sequences that
flank the centromeres of S. cerevisiae's 16 chromosomes are actually
grouped into 8 pairs13. "What we are looking at are the evolutionary
products of some kind of mistake in chromosome pairing that happened
millions of years ago," says Wolfe. Although others have argued that
Wolfe's observations could be the result of multiple duplications,
Wolfe says that his unpublished analysis of other regions of the yeast
genome suggests that it was a single, dramatic event.
A theory with backbone
But what of Ohno's theory that genome duplications were critical to the
evolution of vertebrates? The idea gained support in the late 1980s
with the discovery in mice and humans of four nearly identical gene
clusters that control the development of the body plan, known as the
homeobox, or Hox, genes. Fruitflies - in which Hox genes were first
discovered - and other invertebrates have only a single cluster, but
the order of the genes within it is the same as in the mammalian
clusters. So human Hox genes seem to be the product of two rounds of
duplication of an ancestral Hox cluster14.
When geneticists discovered several other gene clusters that appear
just once in invertebrate genomes but in quadruplicate in vertebrates,
a consensus emerged that the entire genome must have been duplicated
twice in some early ancestor within the vertebrate lineage15. But now
that the human genome has been sequenced in draft form, the debate has
opened up once more.
Austin Hughes, an evolutionary biologist at the University of South
Carolina in Columbia, has found that fewer than 5% of human genes that
have invertebrate homologues appear in quadruplicate. Furthermore, of
134 regions that do have four copies, only 30% are organized into two
clusters of two, as would be expected if two successive genome
duplications had occurred early in vertebrate evolutionary history16.
"To me that closes the book on it," says Hughes.
Not so for Wolfe. Mammalian and bird embryos cannot survive if they are
tetraploid, so any genome duplications in the vertebrate lineage must
have taken place more than 200 million years ago, before either of
these groups had evolved. Such an ancient event would be extremely hard
to spot in today's genomes, Wolfe argues. For one thing, many duplicate
genes - possibly most of them - may have been lost. In yeast, where
evidence of polyploidy is stronger, only 16% of genes seem to have a
surviving homologous partner15. So for Wolfe, whole-genome duplication
may still have played an important role in vertebrate evolution.
Species can also experience sudden reductions in chromosome number, as
is clear from studies of muntjacs, a diminutive genus of deer. The
Chinese muntjac (Muntiacus reevesi) has 23 pairs of chromosomes, but
the Indian muntjac (M. muntjac) has only 3 pairs17. Other members of
the genus have intermediate numbers of chromosomes. Yet the banding
patterns of the chromosomes in all muntjac species suggest that they
contain roughly the same genes.
Shrinking genomes
Wen Wang and Hong Lan of the Chinese Academy of Sciences in Kunming,
Yunnan Province, have produced an evolutionary tree of the seven
muntjac species on the basis of the DNA found in their
energy-generating mitochondria. Their results suggest that the
ancestral muntjac species had a high chromosome number, which decreased
in some lineages as a result of end-to-end fusions between different
chromosomes18. And Fengtang Yang and Malcolm Ferguson-Smith at the
University of Cambridge, UK, have used the colourful technique of
chromosome painting to show that the Indian muntjac chromosome 3 is an
assemblage of seven chromosomes from its Chinese cousin19.
Chromosomes can decrease in size as well as in number - indeed, if
there wasn't some shrinking, duplication events would cause genomes to
grow inexorably over evolutionary time. In fact, Hartl suggests that
spontaneous deletion may be the principal process that determines
genome size. His team estimated the rate of deletions in several
organisms by looking for evidence of excisions within dead transposons,
the ages of which can be estimated by the accumulation of mutations in
their flanking sequences. Hartl found that the fruitfly Drosophila
melanogaster is losing DNA 60 times faster than mammals, which fits
with its much smaller genome size. Hawaiian crickets (Laupala sp.),
which have 11 times more DNA than fruitflies, lose DNA 40 times more
slowly. And the grasshopper Podisma pedestris, whose genome is 100
times bigger than that of Drosophila, loses DNA more slowly still20.
Evolutionary geneticists are now pondering the significance of the
processes that have shaped modern genomes. The more they learn, the
less those vast stretches of non-coding DNA that litter most genomes
seem like just junk. Pericentromeres and subtelomeres may be incubators
for new genes. Duplications may help to generate genetic variation. And
natural selection may continually force genomes to become leaner and
fitter.
Undoubtedly these processes have also left behind heaps of rubbish. But
just as the surface of the Moon holds a record of its impact history in
its craters, those genetic wastelands can serve as records of the
dynamic history of individual genomes. Now equipped with the best maps
yet, the explorers are setting out.
JONATHAN KNIGHT
Jonathan Knight writes for Nature from San Francisco.
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