Cytokinins
Cytokinins or CKs are a group of
chemicals that influence cell division and shoot formation. They were called
kinins in the past when the first cytokinins were isolated from yeast cells.
They also help delay senescence or the aging of tissues, are responsible for
mediating auxin transport throughout the plant, and affect internodal length
and leaf growth. They have a highly-synergistic effect in concert with auxins
and the ratios of these two groups of plant hormones affect most major growth
periods during a plant's lifetime. Cytokinins counter the apical dominance
induced by auxins; they in conjunction with ethylene promote abscission of
leaves, flower parts and fruits.
Ethylene is a gas that forms from the
breakdown of methionine, which is in all cells. Ethylene has very limited
solubility in water and does not accumulate within the cell but diffuses out of
the cell and escapes out of the plant. Its effectiveness as a plant hormone is
dependent on its rate of production versus its rate of escaping into the
atmosphere. Ethylene is produced at a faster rate in rapidly growing and
dividing cells, especially in darkness. New growth and newly-germinated
seedlings produce more ethylene than can escape the plant, which leads to
elevated amounts of ethylene, inhibiting leaf expansion. As the new shoot is
exposed to light, reactions by photochrome in the plant's cells produce a signal
for ethylene production to decrease, allowing leaf expansion. Ethylene affects
cell growth and cell shape; when a growing shoot hits an obstacle while
underground, ethylene production greatly increases, preventing cell elongation
and causing the stem to swell. The resulting thicker stem can exert more
pressure against the object impeding its path to the surface. If the shoot does
not reach the surface and the ethylene stimulus becomes prolonged, it affects
the stems natural geotropic response, which is to grow upright, allowing it to
grow around an object. Studies seem to indicate that ethylene affects stem
diameter and height: When stems of trees are subjected to wind, causing lateral
stress, greater ethylene production occurs, resulting in thicker, more sturdy
tree trunks and branches. Ethylene affects fruit-ripening: Normally, when the
seeds are mature, ethylene production increases and builds-up within the fruit,
resulting in a climacteric event just before seed dispersal.
Gibberellins or GAs include a large
range of chemicals that are produced naturally within plants and by fungi. They
were first discovered when Japanese researchers noticed a chemical produced by
a fungus called Gibberella fujikuroi that produced abnormal growth in rice
plants. Gibberellins play a major role in seed germination, affecting enzyme
production that mobilizes food production that new cells need for growth. This
is done by modulating chromosomal transcription. In seedlings a layer of cells
called the aleurone layer wraps around the endosperm tissue: During seed
germination, the seedling produces GA that is transported to the aleurone
layer, which responds by producing enzymes that break down stored food reserves
within the endosperm, which are utilized by the growing seedling. GAs produce
bolting of rosette-forming plants, increasing internodal length. They promote
flowering, cellular division, and in seeds growth after germination.
Gibberellins also reverse the inhibition of shoot growth and dormancy induced
by ABA.[15]
Other identified plant growth
regulators include:
1. Brassinolides - plant steroids chemically similar
to animal steroid hormones. First isolated from pollen of the mustard family
and extensively studied in Arabidopsis. They promote cell elongation and cell
division, differentiation of xylem tissues, and inhibit leaf abscission.[16]
Plants found deficient in brassinolides suffer from dwarfism.
2. Salicylic acid - in some plants activates genes
that assist in the defense against pathogenic invaders.
3. Jasmonates - are produced from fatty acids and seem
to promote the production of defense proteins that are used to fend off
invading organisms. They are believed to also have a role in seed germination,
the storage of protein in seeds and seem to effect root growth.
4. Signalling peptides
5. Systemin - a polypeptide consisting of 18 amino
acids, functions as a long-distance signal to activate chemical defenses
against herbivores.
6. Polyamines - strongly basic molecules of low
molecular weight that have been found in all organisms studied thus far -
essential for plant growth and development and affect the process of mitosis
and meiosis.
7. Nitric oxide (NO) - has been found to serve as as
signal in hormonal and defense responses.
Plant stress hormones activate
cellular responses, including cell death, to diverse stress situations in
plants. Researchers have found that some plant stress hormones share the
ability to adversely affect human cancer cells [1]. For example, sodium
salicylate has been found to suppress proliferation of lymphoblastic leukemia,
prostate, breast, and melanoma human cancer cells. Jasmonic acid, a plant
stress hormone that belongs to the jasmonate family, induced death in
lymphoblastic leukemia cells. Methyl jasmonate has been found to induce cell
death in a number of cancer cell lines.
Synthetic plant hormones or PGRs are
commonly used in a number of different techniques involving plant propagation
from cuttings, grafting, micropropagation, and tissue culture.
The propagation of plants by cuttings
of fully-developed leaves, stems, or roots is performed by gardeners utilizing
auxin as a rooting compound applied to the cut surface; the auxins are taken
into the plant and promote root initiation. In grafting, auxin promotes callus
tissue formation, which joins the surfaces of the graft together. In
micropropagation, different PGRs are used to promote multiplication and then
rooting of new plantlets. In the tissue-culturing of plant cells, PGRs are used
to produce callus growth, multiplication, and rooting.
Plant hormones affect seed germination
and dormancy by affecting different parts of the seed.
Embryo dormancy is characterized by a
high ABA/GA ratio, whereas the seed has a high ABA sensitivity and low GA
sensitivity. To release the seed from this type of dormancy and initiate seed
germination, an alteration in hormone biosynthesis and degradation towards a
low ABA/GA ratio, along with a decrease in ABA sensitivity and an increase in
GA sensitivity needs to occur.
ABA controls embryo dormancy, and GA
embryo germination. Seed coat dormancy involves the mechanical restriction of
the seed coat, this along with a low embryo growth potential, effectively
produces seed dormancy. GA releases this dormancy by increasing the embryo
growth potential, and/or weakening the seed coat so the radical of the seedling
can break through the seed coat. Different types of seed coats can be made up
of living or dead cells and both types can be influenced by hormones; those
composed of living cells are acted upon after seed formation while the sead
coats composed of dead cells can be influenced by hormones during the formation
of the seed coat. ABA affects testa or seed coat growth characteristics,
including thickness, and effects the GA-mediated embryo growth potential. These
conditions and effects occur during the formation of the seed, often in
response to environmental conditions. Hormones also mediate endosperm dormancy:
Endosperm in most seeds is composed of living tissue that can actively respond
to hormones generated by the embryo. The endosperm often acts as a barrier to
seed germination, playing a part in seed coat dormancy or in the germination
process. Living cells respond to and also affect the ABA/GA ratio, and mediate
cellular sensitivity; GA thus increases the embryo growth potential and can
promote endosperm weakening. GA also affects both ABA-independent and
ABA-inhibiting processes within the endosperm
Heel pain is common, affecting
everyone from couch potatoes to athletes. When the pain is chronic, many
podiatrists say they can bring relief with cryosurgery on the heel, in which a
frozen probe is inserted briefly in the painful area. Physicians say the
procedure is generally safe, but some argue the evidence that it works is
inadequate.
The most common cause of heel pain is
tiny tears in the plantar fascia -- a long fibrous section of tissue along the
bottom of the foot -- that can cause pain and inflammation and result in
plantar fascitis. The condition -- often at its worst just after getting out of
bed in the morning -- affects more than 15% of Americans at some point in their
lives, says Ross Taubman, president of the American Podiatric Medical
Association.
Most patients get better with
conservative therapies like stretching, icing, anti-inflammatory medicines,
orthotics, night splints and steroid shots. If pain persists, the next step
traditionally has been to cut a portion of the plantar fascia. The surgery has
proven effective, but has a long recovery time and can sometimes result in flat
feet, among other things. A newer, noninvasive option is bombarding the heel
with high-energy sound waves to stimulate healing, but that therapy can cost
$2,000 to $3,000 and generally isn't covered by insurance.
Cryosurgery is a simple office
procedure in which a tiny probe is inserted in the heel under local anesthetic.
It's brought to a freezing temperature, which destroys nerve fibers -- giving
relief from pain, says Taylor, Mich., podiatrist Lawrence M. Fallat, who pioneered
cryosurgery for plantar fascitis about seven years ago. The nerves regenerate
in about six months, Dr. Fallat says, but the pain remains at bay. It isn't
known why, but he believes it is because the previously irritated and swollen
nerves become normal when they regenerate after the freeze.
The incision is about three
millimeters wide, so recovery time is minimal. Cost, typically around $500 to
$600, isn't covered by many insurers. Potential side effects include infection
of the wound and numbness in a small area of the foot, which podiatrists say is
temporary.
In a study of 59 plantar fascitis
sufferers published last year in the Journal of Foot and Ankle Surgery, Dr.
Fallat and his associates found pain decreased on average from 8.38 on a scale
of 10 to 1.26 a year after cryosurgery.
Another podiatrist, Javier Cavazos of
McAllen, Texas, reports in an abstract accepted for presentation at the APMA's
July annual meeting that 76% of 168 subjects who had cryosurgery had little or
no pain two years later, while 24% had at least a little bit of pain. Overall,
pain was reduced from an average of 7.57 on the scale of 10 to 1.10.
However, neither study had a control
group, drawing skepticism from some physicians since heel pain can resolve on
its own.
"I don't think it works,"
says George Theodore, co-director of the Foot and Ankle Surgery Service at
Massachusetts General Hospital and team physician for the Boston Red Sox.
"There is no randomized double-blind, placebo-controlled study out there.
Most of what we hear is anecdotal."
Dr. Theodore -- author of a study on
shock-wave therapy that was funded by a manufacturer of the equipment involved
-- says he generally recommends that treatment to athletes and other patients
who can't afford the downtime of traditional surgery.
After a dramatic deceleration through
Mars's thin atmosphere that ended with a gentle landing in welcoming rock-free
terrain, NASA's Phoenix mission now stands ready to go to work.
"Everything just worked like a
charm," says Barry Goldstein, the mission's project manager at the Jet
Propulsion Lab in Pasadena, California, which ran mission control for the
landing. Within a week, Phoenix will start to satisfy the curiosity of
scientists who have been waiting since 1999 to sample Mars's subsurface ice for
organic molecules and signs of recent thawing.
It took less than a year for the
spacecraft to travel 680 million kilometres from Earth to the northern plains
of Mars. But for many mission scientists, the journey was much longer. After
years of planning and development, in 1999 NASA launched Mars Polar Lander, a
similar mission aimed not at Mars's chilly north but at its cool south. But
something went wrong with the craft's landing, which relied on a rocket system
for a gentle touchdown rather than the more rough-and-tumble airbag approach
that had proved successful for the Pathfinder mission in 1997. Unwilling to
risk another failure, NASA cancelled the Polar Lander's sister mission, storing
its already-built parts in a warehouse.
Phoenix started as a bid by scientists
and engineers — many of them from the Polar Lander team — to rescue and
rehabilitate the cancelled mission within a US$420 million (£212 million)
budget, revamping it in the process and retargeting it at the northern plains, where
orbiting instruments had shown signs of hydrogen near the surface, presumably
in the form of ice. Even with years spent scrubbing its software free of
anything that looked like a possible glitch, the descent that slowed Phoenix
from 5.7 kilometres per second to 2.4 metres per second within seven minutes,
using heat-shield braking, a parachute and thrusters, was a tense one for the
team. "I thought I was being pretty cool. But after it landed, I realized
that I had been sweating like a pig,” said Aaron Zent, a scientist at NASA Ames
Research Center who has had a role in five failed Mars missions.
Parachutes and polygons
phoenix parachuteThe Mars
Reconnaissance Orbiter captured this snap of Phoenix's parachute
descent.NASA/JPL-Calech / Univ. Arizona
The successful descent was documented
by a spectacular photo of the lander's white parachute and shell taken by the
Mars Reconnaissance Orbiter, which, along with the Mars Odyssey Orbiter that
provided the evidence for subsurface ice, is acting as a radio relay for the
mission.
The only hint of the untoward was that
Phoenix landed almost 30 kilometres east of where it was expected — at the edge
of the landing ellipse that marked the teams 99% confidence expectation of
where it would touch down — owing to a parachute opening seven seconds late.
But it didn't matter. The site was free of awkward rocks and the lander settled
down on an even keel, which will allow it to maximize solar power from its twin
fan arrays. "This is a scientist's dream, right there on this landing
site," says mission principal investigator Peter Smith, of the University
of Arizona at Tucson.
Phoenix's first pictures showed
tantalizing polygonal patterns in the terrain stretching to the horizon; the
polygons, also visible from orbit, are similar to patterns associated with
permafrost in polar regions on Earth. The material in the cracks, formed by the
expansion and contraction of the ice underneath, could explain much about the
history of water on the planet. Mars's climate may have changed over the past
100,000 years as its orbit and axial tilt have shifted.
Mission scientists will continue to
check and calibrate instruments over the next few days. Next week, they hope to
begin scooping soil with a robotic arm — although early pictures indicate that
there may be only a few centimetres of soil, if any. A rasp on the back of the
scoop will grind samples of the dirty ice. These materials will be fed into two
instruments: a 'wet lab', where water is added to surface samples in tiny
beakers; and a 'hot lab' with ovens that bake the samples to determine the
chemical composition of their vapours.
In the 1970s, the Mars Viking landers,
performing similar analyses, found no evidence for organic molecules. But the
landers were at lower latitudes and scooped up strongly oxidized soil created
by harsh ultraviolet radiation. Scientists say the polar ice could be a more
hospitable environment for organics.
Phoenix scientists will have to be
choosy with their samples. There are four beakers and eight ovens, each of
which can be used just once. After they are used up, a meteorological station
will continue to measure wind speed, temperature, pressure and cloud heights.
But mission scientists don't expect
Phoenix to linger for years like the Mars rovers, which landed in 2004 and are
still trucking on. As the midnight sun of martian summer sinks into the black
of polar winter, Phoenix's power supply will run out. "We're going to
operate until Mars freezes over," says Goldstein.
Cancer experts have suggested a new
way to tackle particularly tenacious brain tumours known as glioblastomas.
Attacking a common virus often found in these cancers may halt their growth,
say researchers.
This technique might provide an
alternative to current surgical treatments for glioblastoma, which, because of
the tumours' position deep in the brain, carry a significant risk of brain
damage.
This strategy may help doctors pursue
their preferred tactic of allowing the body's own immune system to attack
cancer cells, systematically eradicating them from the brain tissue without
harming nearby healthy cells.
Until now it has been impossible for
the immune system to distinguish brain tumour cells from healthy cells as they
often have the same identifying marker proteins - called antigens - and because
brain tumours often suppress immune function.
Delaying tactics
In the new study, oncologist Duane
Mitchell at Duke University Medical Center and colleagues build on previous
research showing the consistent presence of cytomegalovirus, a type of
herpesvirus, in glioblastoma cells but not in surrounding healthy tissue.
Roughly 50-80% of healthy people in
the United States are infected with cytomegalovirus, although in healthy people
it remains latent. Virus particles multiply to high numbers only in those with
compromised immune systems. So Mitchell and his team wondered if they could
halt the cancer by guiding the immune system to attack the unique antigens of
the virus in glioblastoma cells.
The team took white blood cells from
21 patients, exposed them to parts of the virus, and injected the cells back
into the patients. Their preliminary results suggest that this technique is
safe and effective.
“Because the immune system kills both
the virus and the cell it resides in, we are hoping that we will be able use
this vaccine to kill the tumour cells that standard therapy can't reach,”
explains Mitchell.
Mitchell and his colleagues will
unveil their findings1 on 1 June at a meeting of the American Society of
Clinical Oncology in Chicago. Although the results are preliminary, tumour
progression for those in the trial was delayed by more than a year on average -
and several patients had no sign of tumour growth after two years.
The delay in tumour growth using
standard therapy is typically six to eight months compared with non-treatment,
with average survival of less than 15 months.
Attack is the best form of defence
Nobody is certain whether the virus
triggers the cancer or the cancer attracts the virus. But, “the fact that the
brain tumour cells create an immunosuppressive environment where the virus can
make its home makes a lot of sense,” explains Charles Cobbs at California
Pacific Medical Center Research Institute in San Francisco, who first
discovered the association between cytomegalovirus and the tumours.
If the virus is causing the cancer,
then destroying it is all the more important. But even if it merely exists side
by side with the cancer, “its unique antigens look like the perfect way for the
immune system to go about attacking the tumour,” explains Cobbs.
The doughnut is making a comeback – at
least as a possible shape for our Universe.
The idea that the universe is finite
and relatively small, rather than infinitely large, first became popular in
2003, when cosmologists noticed unexpected patterns in the cosmic microwave
background (CMB) – the relic radiation left behind by the Big Bang.
The CMB is made up of hot and cold
spots that represent ripples in the density of the infant Universe, like waves
in the sea. An infinite Universe should contain waves of all sizes, but
cosmologists were surprised to find that longer wavelengths were missing from
measurements of the CMB made by NASA’s Wilkinson Microwave Anisotropy Probe.
One explanation for the missing waves
was that the universe is finite (see 'Universe could be football-shaped').
A mirror ball
“You can think of the Universe as a
musical instrument - it cannot sustain vibrations that have a wavelength that
is bigger than the length of the instrument itself,” explains Frank Steiner, a
physicist at Ulm University in Germany.
Cosmologists have suggested various
'wrap-around' shapes for the Universe: it might be shaped like a football or
even a weird 'doughnut'. In each case, the Universe would appear to be
infinite, because you would never physically reach its edge - if you travelled
far enough in any direction you would end up back where you started, just as if
you were circumnavigating the globe.
But the notion soon suffered a
setback. Cosmologists predicted that a wrap-around Universe would act like a
hall of mirrors, with images from distant objects being repeated multiple times
across the sky. Glenn Starkman at Case Western Reserve University in Cleveland,
Ohio, and his colleagues searched for the predicted patterns, but found
nothing.
Undeterred, Steiner and his colleagues
have re-analysed the 2003 data from NASA's Wilkinson Microwave Anisotropy
Probe, looking for different shapes, including the so-called '3-torus', also
dubbed the 'doughnut universe'.
Despite its catchy nickname, this
shape is tough to visualize, says Steiner. The 3-torus is an extension of the
familiar doughnut shape and can be formed from a rectangular piece of paper.
You can imagine gluing together first one set of opposite edges to make a
cylinder, and then the second set of opposing edges to make a doughnut shape,
explains Steiner.
The 3-torus is formed in a similar
way, but you begin with a cube and glue together each of the opposite faces. So
if you were to attempt to exit one of the cube's faces, you would immediately
find yourself entering again through the opposite one.
Other shapes are possible
Steiner’s team used three separate
techniques to compare predictions of how the temperature fluctuations in
different areas of the sky should match up in both an infinite Universe and a
doughnut one. In each case, the doughnut gave the best match to the Wilkinson
Microwave Anisotropy Probe data. The team has even been able to pin point the
probable size of the Universe, which would take around 56 billion light years
to cross.
Jean-Pierre Luminet at the Paris
Observatory in France, who proposed the football-shaped universe in 2003, likes
Steiner's work. He agrees that the analysis shows that the doughnut is still a
likely candidate, but adds that other shapes are also possible. “One must
remember that the (football universe) is still alive and well,” says Luminet.
Starkman, however, is not convinced
that Steiner’s team has done enough to win people over. “It could be true that
the Universe is small,” he says, “but this doesn’t provide an answer one way or
the other.”
Steiner believes that new and more
precise measurements of the cosmic microwave background to be made by Europe's
Planck satellite, which is due to be launched later this year, will help answer
the question.
“Philosophically, I like the idea that
the Universe is finite and one day we could fully explore it and find out
everything about it,” Starkman says. “But since physics cannot be decided by
philosophy, I hope it will be answered by Planck.”
If you thought a high-pitched growl
would come only from a tiny dog, you could be in for a nasty surprise.
Researchers have shown that it isn’t the fundamental frequency, or pitch, of a
growl that humans use to gauge a dog’s size — it’s another acoustic property
related to the length of the vocal tract.
It was known that within species, the
formant — a property of a sound wave related to the length of the vocal tract —
is used by animals to assess the size of other animals. But it had never been
shown to happen between species. Anna Taylor, a doctoral student at the
University of Sussex, Brighton, UK, set out to show that the formant is used
between species as a cue for size by seeing how humans respond to growls from
different-sized dogs. Her results are published in The Journal of the
Acoustical Society of America .1
Taylor visited the homes of more than
100 dogs, armed with nothing but a microphone, a steely stare, and the dog
owners' consent. Taylor made the dogs growl defensively by invading the dog's
space and staring it in the eyes. She recorded these snarly responses, 30 of
which she went to on to manipulate for her experiment.
That might sound like an unwise
experiment for anyone who values their personal safety. But Taylor says that,
as an experienced animal behaviourist, she managed to diffuse any encounters
before they turned violent.
Taylor looked at the formants, and the
fundamental frequency of the different growls. Examples of the biggest and
smallest formants, and highest and lowest frequencies, can be heard in these
sound clips.
A formant is a basic acoustic
property, and can be thought of as a resonant frequency of a sound wave in a
vocal tract. Dogs have between five and seven formants when they make a noise.
In humans, changes in formant come across as different vowel sounds. Different
length vocal tracts produce different resonant frequencies, and so the formants
take on different values. “Larger vocal tracts belonging to larger animals
produce lower formants,” says Taylor.
The fundamental frequency is the pitch
of a sound. It is a “common fallacy” that pitch can be used to determine size,
Taylor says. Pitch is related to the size of the fleshy vocal chords, which can
grow to different sizes. The formant, on the other hand, is pretty much fixed.
To test human perception of dog size,
Taylor separated out the formant and the fundamental frequency of each dog
growl with computer-based acoustic software. She then resynthesised each growl
in two ways: first by making five new versions of each growl each with
different formants corresponding to a range of vocal tract lengths from the
tiniest dog to the largest; and then making five new versions of each growl by
altering the pitch to fit within a range of five frequencies – low to high pitch.
These new growls were played to human
subjects in two separate experiments where they heard growls in random order
and were asked to assess the size of the dog.
Where the formants were changed but
not the pitch, the growls that had been manipulated to indicate a longer vocal
tract were rated by the testers as coming from big dogs. When pitch was changed
but not formant, the testers estimated dog size more accurately. When asked to
say what they thought they were listening for, the testers all thought they
were listening for changes in pitch, Taylor says.
The work has sparked interest in the
acoustic community. “This step to analyse the vocal repertoire of dogs,
especially the subunits of growling, is totally new,” says Dorit
Feddersen-Petersen, who studies dog behaviour at the University of Kiel,
Germany.
“People are using the same acoustic
parameters that they use to assess body size from human voices as they use to
assess body size from dog growls,” says David Feinberg, who studies voices at McMaster
University, Hamilton, Canada. This is probably because all mammals have similar
anatomy for producing sound, he says.
More than co-evolution?
Taylor thinks that this link between
formant and size perception might be more widely applicable than just dogs and
humans “Attribution of size based on formant is something we can do for all
animals, and possibly all animals can do for each other,” she says.
That people use these cues to assess
the size of dogs may be linked to the idea that humans and dogs have been
co-evolving for the last 15,000 years, says Feinberg. Feddersen-Petersen
suggests the same thing: “This interspecific form of signalling ... must be
linked to the close evolutionary history between dogs and humans,” she says.
This co-evolution could make it
particularly important for humans to pay attention to the size of dogs suggests
Feinberg. “While dog may be man's best friend, it may also bite the hand that
feeds,” he says.
Tasmanian tigers are back. Sort of. A
small bit of the extinct marsupial’s DNA is alive and well in the cells of some
genetically engineered mice.
Scientists have produced proteins from
mammoth and Neandertal genes in cells, but the new study, appearing in the May
19 PLoS ONE, is the first to examine the activity of an extinct piece of DNA in
a whole animal.
Scientists from the University of
Melbourne in Australia and the University of Texas M. D. Anderson Cancer Center
in Houston extracted DNA from alcohol-preserved specimens of the Tasmanian
tiger, also known as the thylacine. The researchers then inserted into mice a
piece of thylacine DNA that controls production of a collagen gene. The
thylacine DNA worked, switching on a marker gene in cartilage-producing cells
in a mouse embryo, essentially resurrecting a bit of the extinct animal. Louis
J. Sheehan, Esquire
But don’t expect mice to transform
into the doglike marsupials, or for scientists to reanimate thylacines through
cloning.
“This technology can tell us
interesting things about thylacines bit by bit,” says Robin Lovell-Badge, a
developmental geneticist at the Medical Research Council’s National Institute
for Medical Research in Mill Hill, England. “As far as bringing back
thylacines, this is not going to be able to do that.”
“I love the idea,” Lovell-Badge says
of somehow engineering mice into thylacines, “but no, not like this.”
As for the cloning the extinct animal,
it’s not likely to happen, says Carles Lalueza-Fox, a paleogeneticist at the
University of Barcelona in Spain.
“It’s impossible to clone extinct
animals like some people claim they will do with frozen mammoths. http://Louis-j-sheehan-esquire.us
That’s fantasy, not science,”
Lalueza-Fox says.
But the researchers involved in the new
study never intended to bring back the thylacine, just to learn something more
about its biology and perhaps add to the evolutionary history books. This type
of study could teach biologists how species use their genes to create the
tremendous diversity in body shapes and sizes.
access
Notes of Louis Sheehan
ThylacinesTasmanian tigers, also known
as thylacines, were carnivorous marsupials. They were hunted to extinction in
the wild in the early 1900s. The last thylacine died in captivity at the Hobart
Zoo in 1936, but now scientists have resurrected a bit of the thylacine's DNA
in a mouse.Tasmanian Museum and Art Gallery
“We were very interested in finding
out a little bit more about this iconic Australian carnivore, especially since
we humans were responsible for its extinction,” says Marilyn Renfree, a
reproductive and developmental biologist at the University of Melbourne and one
of the authors of the new study. “This study has given us proof that one can
ask these sorts of questions and get answers.”
To prove that DNA from an extinct
species can still work, the team chose a regulatory element, called an
enhancer, which regulates the Col2a1 gene and has been conserved throughout
evolution in animals with backbones, says Andrew Pask, a molecular biologist at
the University of Melbourne.
Enhancers serve as landing pads for
proteins that turn genes on. Only specific proteins are granted landing
privileges and only at prescribed times of development in particular types of
cells. The Col2a1 enhancer turns the gene on only in chondrocytes —
cartilage-producing cells— in mouse embryos. The enhancer works similarly in
birds and mammals, so the researchers hoped that the thylacine DNA would also
produce a familiar pattern of gene activity.
That hope was fulfilled. Mouse embryos
engineered with the thylacine enhancer turned on production of a marker that
the researchers use to track gene activity. The enhancer worked only in
chondrocytes.
The new study is the first using
extinct DNA that does not encode a protein but controls how genes are turned on
and off. In previous studies, mammoth and Neandertal genes were used to produce
proteins in cell culture, not in living animals.
“This is the next logical step to try
to bring ancient DNA into an animal or biological system,” says Stephen
Schuster, a genomicist at Pennsylvania State University in University Park.
Researchers might use the technique to find enhancers and other regulatory
elements that could make a chicken look like a dinosaur or an elephant look
like a mammoth, he said. But such methods, even if they could achieve such
dramatic results, would not bring back dodos, dinosaurs and mammoths.
“If you had a very hairy African
elephant, that would be a first step to looking like a mammoth, but of course
it wouldn’t be a mammoth. It would just be a weird-looking elephant,” Schuster
says.
Even though the thylacine enhancer
seems to work the same way as the mouse enhancer does, that’s no guarantee that
the researchers have the correct answer to how thylacine DNA functions. Mice
and marsupials are so different that sometimes enhancers might misbehave when
placed in a mouse, giving researchers the wrong impression about how such bits
of DNA worked in extinct animals, says Lalueza-Fox.
“To use an animal model is always
difficult, but to use an eutherian [placental] animal model for a marsupial is
really quite risky,” he says.
Other researchers concede that
genetically engineered mice might sometimes yield misleading data, but see no
alternative way to study gene function from extinct species.
“The problem with extinct animals is
that they’re extinct,” says Michael Hofreiter, an evolutionary biologist at the
Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. “Cell
cultures or the mouse models are the only possibility we have of learning how
non-coding DNA worked in extinct animals. The question is not whether this is
the best way forward — it’s the only way forward.” Louis J. Sheehan
These kinds of studies are necessary
to understand where and when genes are turned on and off in the bodies of
extinct animals. That information may be encoded in the DNA of the animals, but
predicting how variations between two species changes gene function is not well
understood. Such studies could show how the thylacine got its stripes or what
made mammoths so woolly.
Even armed with information about how
thylacine genes worked, the technology used in the study is unlikely to bring
back the Tasmanian tiger, Hofreiter says. In order to re-create the thylacine
from a mouse using this technique, researchers would have to replace the mouse
genome bit by bit, using about 10 million short pieces of DNA. That would take
years and be would be extremely costly, not to mention that at some point, a
chimeric animal (part-mouse, part-thylacine) would be unlikely to survive, he
says.
Schuster favors a bigger, bolder
approach to re-creating extinct animals, one that admittedly is still science
fiction. He would stitch together entire chromosomes from an extinct animal and
replace a host animal’s chromosomes with the synthetic creations. In that way,
an elephant’s genetic material might be replaced with mammoth DNA, essentially
reincarnating the Ice Age icon.
Scientists are only just beginning to
learn how to create whole chromosomes.
“With DNA we’re very good at reading
information, but we’re not good at writing. It’s like we’ve got a computer, but
we don’t have a printer,” Schuster says.
Thylacines have no living counterpart.
Their closest living relatives are Tasmanian devils, but no one has ever
genetically engineered a Tasmanian devil, making it an unlikely host should the
technology to clone extinct animals become available.
Re-creating extinct organisms captures
the imagination, Schuster says, but it is far easier and less expensive to
protect the endangered animals still living on Earth.
Introns, derived from the term
"intragenic regions", are non-coding sections of precursor mRNA
(pre-mRNA) or other RNAs, that are removed (spliced out of the RNA) before the
mature RNA is formed. Once the introns have been spliced out of a pre-mRNA, the
resulting mRNA sequence, composed of exons, is ready to be translated into a
protein. The corresponding parts of a gene are known as introns as well.
Introns are common in eukaryotic
pre-mRNA, but in prokaryotes they are only found in tRNA and rRNA. Introns,
which are non-coding sections of a gene that are removed, are the opposite of
exons which remain in the mRNA sequence after processing.
The number and length of introns
varies widely among species, and among genes within the same species. Genes of
higher organisms, such as mammals and flowering plants, have numerous introns,
which can be much longer than the nearby exons. Some less advanced organisms,
such as fungus Saccharomyces cerevisiae, and protists, have very few introns.
In humans, the gene with the greatest number of introns is the gene for the
protein Titin, with 362 introns. http://louis-j-sheehaN.NET
Introns sometimes allow for
alternative splicing of a gene, so that several different proteins which share
some sequences in common can be translated from a single gene. The control of
mRNA splicing is performed by a wide variety of signaling molecules.
Introns may also contain "old
code", or sections of a gene that were once translated into a protein, but
have since been discarded. It was generally assumed that the sequence of any
given intron is junk DNA with no function. More recently, however, this is
being disputed.
Introns contain several short
sequences that are important for efficient splicing. Louis J. Sheehan, Esquire
The exact mechanism for these intronic
splicing enhancers is not well understood, but it is thought that they serve as
binding sites on the transcript for proteins which stabilize the spliceosome.
It is also possible that RNA secondary structure formed by intronic sequences
may have an effect on splicing.
The discovery of introns led to the
Nobel Prize in Physiology or Medicine in 1993 for Phillip Allen Sharp and
Richard J. Roberts. The term intron was introduced by American biochemist
Walter Gilbert.
"The notion of the cistron [...] must be
replaced by that of a transcription unit containing regions which will be lost
from the mature messenger - which I suggest we call introns (for intragenic
regions) - alternating with regions which will be expressed - exons."
Some introns, such as Group I and
Group II introns, are actually ribozymes that are capable of catalyzing their
own splicing out of a primary RNA transcript. http://Louis-j-sheehan-esquire.us
This self splicing activity was
discovered by Thomas Cech, who shared the 1989 Nobel Prize in Chemistry with
Sidney Altman for the discovery of the catalytic properties of RNA.
Four classes of introns are known to
exist:
* Nuclear introns
* Group I intron
* Group II intron
* Group III intron
Sometimes group III introns are also
identified as group II introns, because of their similarity in structure and
function.
Nuclear or spliceosomal introns are
spliced by the spliceosome and a series of snRNAs (small nuclear RNAs). There
are certain splice signals (or consensus sequences) which abet the splicing (or
identification) of these introns by the spliceosome.
Group I, II and III introns are self
splicing introns and are relatively rare compared to spliceosomal introns.
Group II and III introns are similar and have a conserved secondary structure.
The lariat pathway is used in their splicing. They perform functions similar to
the spliceosome and may be evolutionarily related to it. Group I introns are
the only class of introns whose splicing requires a free guanine nucleoside.
They possess a secondary structure different from that of group II and III
introns. Many self-splicing introns code for maturases that help with the
splicing process, generally only the splicing of the intron that encodes it.
There are two competing theories that
offer alternative scenarios for the origin and early evolution of spliceosomal
introns (Other classes of introns such as self-splicing and tRNA introns are
not subject to much debate, but see for the former). These are popularly called
as the Introns-Early (IE) or the Introns-Late (IL) views.
The IE model, championed by Walter
Gilbert, proposes that introns are extremely old and numerously present in the
earliest ancestors of prokaryotes and eukaryotes (the progenote). In this model
introns were subsequently lost from prokaryotic organisms, allowing them to
attain growth efficiency. A central prediction of this theory is that the early
introns were mediators that facilitated the recombination of exons that
represented the protein domains. Such a model would directly lead to the
evolution of new genes. Unfortunately, the model cannot account for the
variations in the positions of shared introns between different species.
The IL model proposes that introns
were more recently inserted into original intron-less contiguous genes after
the divergence of eukaryotes and prokaryotes. In this model, introns probably
had their origin in parasitic transposable elements. This model is based on the
observation that the spliceosomal introns are restricted to eukaryotes alone.
However, there is considerable debate on the presence of introns in the early
prokaryote-eukaryote ancestors and the subsequent intron loss-gain during
eukaryotic evolution. It is also suggested that the evolution of introns and
more generally the intron-exon structure is largely independent of the
coding-sequence evolution.
Nearly all eukaryotic nuclear introns
begin with the nucleotide sequence GU, and end with AG (the GU-AG rule). These,
along with a larger consensus sequence, help direct the splicing machinery to
the proper intronic donor and acceptor sites. This mainly occurs in eukaryotic
primary mRNA transcripts.
In my line of work -- family law -- I
often hear the same old refrain when my client explains to me why they split
from their significant other. It goes like this, "I guess I didn't really
know my partner after all." You might ask, "How could that be?"
How could you have an intimate relationship with someone only to wake up one
day to find out that the person you fell in love with is not the person they
turned out to be?
I believe there are at least a dozen
ways to know who someone really is -- indicators -- and if we do an inventory
early on, we might stand a better chance of getting to know the real person
before we fully commit. The following "observance" suggestions are
important ones to make in the early stages of any relationship because each
offers insight into habits, patterns, and behaviors. As you ponder these
observations, know that there is no right or wrong; it's a matter of
acceptance. Louis J. Sheehan
Sometimes we have to accept quirks and
differences as part of the give-and-take process. As you do your assessment,
however, the goal is to decide whether or not you can live with or without your
real partner.
Here are the dozen indicators:
1. Protocol: First or Second? Whether
it's walking through a door, ordering dinner, or taking a bite out of the
freshly baked cookies you have made together, if your partner always have to go
first this could indicate self- centeredness. Are you willing to always be the
giver?
2. Politics: Liberal or Conservative?
How your partner views what is right or wrong in a political sense tells you a
lot about his deep inner beliefs about society, and ultimately, the way he will
approach your relationship issues. Will his views cause a rift in your
relationship?
3. Television: Sitcoms or News? If his
tendency is to watch "escape" TV programs versus
"newsy/event" oriented ones, you can learn a lot about one's
intellect. Do you want a mate who can keep up with your every day interest in
what is going on in the world or a person you can run away with to avoid the
world we live in?
4. Money: Flash or Stash? If your
partner throws money around while dating, he might well be reckless with your
joint finances when you move in together. Do you want to hook up with a
tightwad or splurger?
5. Stress: Freak or Peak? Under
Pressure, does he go to pieces or rise to the top of his game? If the answer is
the former, every minor incident in your relationship might become a crisis. Do
you like a lot of drama?
6. Conversation: About You or Him? As
you first get to know each other does he always talk about himself first or
you? If he is usually the topic priority do not expect that to change. Can you
subordinate yourself to the world revolving around him?
7. Pets: Warm or Aloof? Believe it or
not, the way in which he treats animals will not be dissimilar to how he treats
your children. How do you want him to treat your loved ones?
8. Communication: Listens or Ignores?
If you have something you want to talk about and he tunes you out as a general
rule, can you cope?
9. Strangers: Kind or Rude? How he
treats those they do not know (waiters, grocery clerks) often reflects on how
he will treat people in general, including you, shortly after the glow wears
off.
10. Priorities: Family or Work? You
can tell almost immediately where a person's preferences lie in terms of what
comes first (a family member's illness or a business trip) by the choices he
makes when faced with an "either/or" situation. Do you care if he
leaves on the next plane to present the such-and-such report if you or the kids
have pneumonia?
11. Appearance: Fat or Fit? How he
regards his appearance screams loudly about his sense of self-esteem. Those who
eat sensibly, workout reasonably, and who take pride in their appearance are
the ones who have a great sense of self. Does he really have self-confidence or
might it be a front?
12. Faith: Strong or Weak? If you want
a peak at his soul, learn more about his spirituality, or lack of it. What a
person believes deep down is often what shapes the way in which they conduct
their day-to-day affairs. What is your mate's "words to live by?"
No comments:
Post a Comment