Why do all cells have the complete genome? [Pharyngula]


Ophelia has summarized a series of science questions Richard Dawkins asked on Twitter. Hey, I thought, I have answers to lots of these — he probably does, too — so I thought I’d address one of them. Maybe I can take a stab at some of the others another time.


I like this one, anyway:



Why do cells have the complete genome instead of just the part that’s needed for their function? Liver cells have muscle-making genes etc.



My short answer: because excising bits of the genome has a high cost and little benefit, and because essentially all of the key exaptations for multicellularity evolved in single-celled organisms, where modifying the DNA archive would have serious consequences for all the daughter cells.


This is an interesting issue, though: different kinds of cells in the same organism express genes that are qualitatively and quantitatively different. Here’s a set of nice graphs in which the relative fraction of different classes of genes in gene transcripts in different cell types were measured. Notice in the list of biological processes that a lot of them, such as the genes involved in transcription and translation and metabolism, are going to be used in all cells, but some, such as neuron-specific or testis-specific genes, are only going to be expressed in some cells.


(A) Pie graphs show estimated fraction of cellular transcripts deriving from genes belonging to a set of top-level Gene Ontology Biological Process categories for 7 human tissues and 1 cell line. Fractions were estimated from read density (RPKM) of Ensembl transcripts for each gene. Names of categories, distribution of transcriptome fraction across the samples (each line is a sample), and the coefficients of variation are shown at right. Biological processes with significantly higher or lower densities in individual tissues and cell lines are denoted by arrows. (B) FRACT analysis of sub-categories of the top-level ‘Development’ category in brain and testes.

(A) Pie graphs show estimated fraction of cellular transcripts deriving from genes belonging to a set of top-level Gene Ontology Biological Process categories for 7 human tissues and 1 cell line. Fractions were estimated from read density (RPKM) of Ensembl transcripts for each gene. Names of categories, distribution of transcriptome fraction across the samples (each line is a sample), and the coefficients of variation are shown at right. Biological processes with significantly higher or lower densities in individual tissues and cell lines are denoted by arrows. (B) FRACT analysis of sub-categories of the top-level ‘Development’ category in brain and testes.



It also gets complicated because some genes are found in very different forms: there is a kind of universal myosin, myosin I, for instance, that is expressed in all cells as part of the intracellular transport machinery, and then there is a myosin variant, myosin II, that is expressed only as a part of the contractile machinery in muscle. So you might think that it would be more efficient for a skin cell to simply cut out and throw away Myosin II, since it’ll never use it, and keep Myosin I.


But how does the cell determine which genes it will never use? Where does it draw the line? All those testis development genes, for example — I never used many of them until I hit puberty. Wouldn’t it have been terrible if my young toddler testicles threw out a set of unused genes, and then a dozen years later discovered that they had a use, after all? There are a great many genes regulated by timing and signals, and as can be seen in that figure above, every cell has a different expression profile. There are a variety of cells in my skin that are busy replicating and making keratin proteins as a matter of course, but they only switch on cellular repair mechanisms if I cut myself. There are also many genes that get reused in complicated ways, too: the gene even-skipped is first switched on as part of the segment forming process in flies, but it later is switched on again in making neuroblasts, and later still is expressed in axons during pathfinding. Cells would rather recycle genes than throw them away.


These properties are not unique to us mammals, either. Bacteria regulate which genes are turned off and on, too — they change their biochemical behavior in response to signals in their environment. The ability to switch on and switch off genes, without eliminating the DNA, is a solved problem. Life figured that one out a few billion years ago. Key molecules required for multicellular patterns of gene expression first evolved in bacteria — they worked out how to have a cell with the same genetic material behave differently in different circumstances. We came about ready made with a toolkit equipped to have one set of genes turned on in livers, and a different set turned on in muscles, easy.


But, you might think, wouldn’t it be so much more cost-efficient if cells in multicellular organisms just got rid of genes they’d never turn on in their lifetime, once they’ve committed to a certain tissue type? Muscle cells will never make sperm recognition proteins, and liver cells won’t ever have to lift weights, and you could probably cut the amount of DNA in differentiated cells in half with no effect on function.


But that’s penny-wise accounting. In bacteria, only about 2% of the cell’s energy budget is invested in replication — so removing a bit of DNA here and there is only going to shave a tiny amount off the cost of cell division. On the other hand, an amazing 75% is spent on transcribing and translating genes, so efficient mechanisms of simply turning off unused genes reaps huge savings for the cell. Evolving a complex process to pare away unused DNA in terminally differentiated cells simply does not make sense energetically, while simply taking advantage of an already fully implemented and refined process for regulating gene expression…heck, that’s what evolution does best, reusing what’s already there.


By the way, not all cells carry the complete genome: there are also a few cases where the DNA of an organism is modified — the CRISPR system in bacteria, and the somatic recombination system used in vertebrates to generate diverse immunoglobulins. In both of those cases, though, it’s not a mechanism to cut away unused DNA. It’s a specialized process to create variation during an organism’s lifetime to cope with environmental challenges.




Lane N, Martin W. (2010) The energetics of genome complexity. Nature 467(7318):929-34.


Ramsköld D1, Wang ET, Burge CB, Sandberg R (2009) An abundance of ubiquitously expressed genes revealed by tissue transcriptome sequence data. PLoS Comput Biol 5(12):e1000598. doi: 10.1371/journal.pcbi.1000598.



Friday Cephalopod: I’m not the only one flying [Pharyngula]


Today’s Creation Moment

The Flower that Favors Bumblebees

Matthew 6:28-29

“And why take ye thought for raiment? Consider the lilies of the field, how they grow; they toil not, neither do they spin: And yet I say unto you, That even Solomon in all his glory was not arrayed like one of these.” The tropical looking flower Virginia Meadow Beauty offers some rare tricks for those who would pollinate it. A honeybee can poke around the flower all day and never get any pollen from the gaudy pink flowers. In fact, researchers report that honeybees don’t seem to know what to do with the flowers. Rather, the Virginia Meadow Beauty is pollinated by bumblebees, not honeybees. The pollen of a newly opened pink flower is good only for that day. But the flowers stay open for several days. It signals the bumblebees that the pollen in old flowers are not good by changing colors. Yet, the spent flowers are serving one more purpose. Researchers report that large displays, even if mostly spent flowers, attract more bumblebees than small displays of all fresh flowers.

How is it that the bumblebee can get the pollen and the honeybees can’t? They just buzz. And when a bumblebee buzzes, the flower ejects its pollen at 30 times the force of gravity – a force greater than any astronaut must endure! It’s not that the bumblebee gets the pollen because it is larger than a honeybee; no, even bumblebees no larger than the honeybee’s head can get the pollen. It’s the frequency of buzzing. The Lord has abundantly provided for the Meadow Beauty. And He has provided for your forgiveness and salvation in His Son, Jesus Christ.

Prayer:

I thank You, Lord, that You so generously provide for all Your creatures. Increase my faith that You will also provide me with all I need, beginning with salvation. Amen.



Author Nick Harkaway on Improvised Grenades and ‘Existential Pulp’


Nick Harkaway

Chris Close Photography



Nick Harkaway is the author of several popular books that straddle the border of realism and science fiction, particularly his debut novel The Gone-Away World , in which a scientific experiment gone wrong obliterates any firm sense of reality. Harkaway is fascinated by the ways in which reality is stranger than most people want to admit, and he’s frustrated that so much contemporary fiction fails to grapple with that strangeness. In particular he’s troubled that so many authors shy away from writing about new technology, even something as simple and familiar as cell phones.


“Quite a lot of the time you’re talking about an artificially constructed 1993, except with everything else being now,” Harkaway says in this week’s episode of the Geek’s Guide to the Galaxy podcast. “A lot of novels that people think of as being ‘real’ are actually basically alternative reality fiction, designed to be in an atechnological world.”


He admits that it can be a challenge to dramatize stories about people talking online, but feels that since our lives are bound inextricably with the technology that surrounds us, novelists can’t hope to probe the human condition unless they’re keeping pace with the latest science, such as experiments that network together the brains of rats.


“You could walk from one end of my country to the other without finding, as far as I know, anything being written as a consequence of that,” says Harkaway. “Certainly outside of science fiction you’re not going to hear a mention of it.”


Listen to our complete interview with Harkaway in Episode 115 of Geek’s Guide to the Galaxy (above). Then stick around after the interview as guest geeks John Joseph Adams, Matt London, and Rob Bland join host David Barr Kirtley to discuss the new Marvel movie Guardians of the Galaxy .


Nick Harkaway on writing existential pulp:


“There’s a taxonomical debate to be had about whether [my fiction] is classically science fiction, and io9 called it ‘existential pulp,’ which I love … Tigerman is definitely full of a sense of worry about what it means to be a dad, and how to be a good person, and all the rest of it, and so it belongs in that [existential] category. And then of course at the same time my pulp roots are showing. Here’s all this serious stuff about global geopolitics and the bad ways we behave overseas, and about being a father and trying to do the right thing, and how do you become a new person when your old life has come to an end. But the answer is you put on a superhero suit and you go fight crime. The thing is, though, I would do dumber things than that for my kids if that’s what they needed me to do. I think we all would.”


Nick Harkaway on improvised grenades:


“It’s true about a lot of powders with a very fine grain size—custard powder is one, pepper is another—that if you put a small amount of them in a box and shake it up, and then throw in a match, you get a big ‘whoomph’ … Certainly you would get a respectable flash and a bang out of that. Whether you’d get any serious percussive force I don’t know … I have a tendency with things like that to work something which is approximately possible under the right circumstances and just let it go, because the thing that I definitely am not is a hard science guru. My scientific qualifications are relatively scant. I like science, I try really hard to educate myself about it, but in the end if something has to go ‘boom’ and it would probably only go ‘fwoosh,’ I am relatively unconcerned about that, which is a sin, but not I think a grave one.”


Guardians of the Galaxy Panel


John Joseph Adams on the comic book backstory of Thanos:


“Basically the Infinity Gems—or as they’re called in the Marvel Cinematic Universe the ‘Infinity Stones’—they’re these six stones that have almost magical abilities, so there’s the Soul Gem and the Power Gem, and they all give a person godlike powers. And so Thanos goes around and collects them all … Thanos is doing this because he’s courting Death. And when I say ‘Death,’ I mean the actual personification of death, the character of Death in the Marvel universe, sort of like the goddess of death. And to try to impress her, he decides he’s going to exterminate half the sentient life in the universe … One of the things that really makes him a compelling villain is that he almost has this sense that he doesn’t deserve it, and so he sets up his own demise. Because the thing is he’s grabbing ultimate power in most of these cases, so they almost have to do that in order to give the heroes any chance to defeat him.”


Matt London on the generic nature of Guardians of the Galaxy:


“I am completely done with prison breaks in sci-fi movies … Just a couple months ago there was a prison break scene in a Marvel movie, in the new X-Men movie. Is this the only thing that we can do as our second act? It’s so boring and tedious. I’ve just seen it so many times now … And then the other thing—sorry to get all narrative structure on people—but as soon as they find the stone and realize that the stone is what it is, I’m like, ‘OK, so now the bad guys are going to show up, and they’re going to have a huge action sequence, and fifteen minutes from now the good guys are going to get beaten down, the bad guys are going to get the stone, and all hope is going to be lost. Watch.’ And then over the next twenty minutes that’s exactly what happened. Everything is so completely predictable and by-the-numbers. We’ve seen this movie before.”



Do gut bacteria rule our minds? In an ecosystem within us, microbes evolved to sway food choices

It sounds like science fiction, but it seems that bacteria within us -- which outnumber our own cells about 100-fold -- may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.



In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.


Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem -- our digestive tracts -- they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.


While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.


"Bacteria within the gut are manipulative," said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper." "There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not."


Fortunately, it's a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.


"Our diets have a huge impact on microbial populations in the gut," Maley said. "It's a whole ecosystem, and it's evolving on the time scale of minutes."


There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.


Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.


"Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good," said Aktipis, who is currently in the Arizona State University Department of Psychology.


In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.


Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?


The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.


"Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating," the authors wrote.


The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago. Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.


In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.


"Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health," she said.


The co-authors' BioEssays study was funded by the National Institutes of Health, the American Cancer Society, the Bonnie D. Addario Lung Cancer Foundation and the Institute for Advanced Study, in Berlin.



Harnessing the power of bacteria's sophisticated immune system

Bacteria's ability to destroy viruses has long puzzled scientists, but researchers at the Johns Hopkins Bloomberg School of Public Health say they now have a clear picture of the bacterial immune system and say its unique shape is likely why bacteria can so quickly recognize and destroy their assailants.



The researchers drew what they say is the first-ever picture of the molecular machinery, known as Cascade, which stands guard inside bacterial cells. To their surprise, they found it contains a two-strand, unencumbered structure that resembles a ladder, freeing it to do its work faster than a standard double-helix would allow.


The findings, published online Aug. 14 in the journal Science, may also provide clues about the spread of antibiotic resistance, which occurs when bacteria adapt to the point where antibiotics no longer work in people who need them to treat infections, since similar processes are in play. The World Health Organization (WHO) considers antibiotic resistance a major threat to public health around the world.


"If you understand what something looks like, you can figure out what it does," says study leader Scott Bailey, PhD, an associate professor in the Bloomberg School's Department of Biochemistry and Molecular Biology. "And here we found a structure that nobody's ever seen before, a structure that could explain why Cascade is so good at what it does."


For their study, Bailey and his colleagues used something called X-ray crystallography to draw the picture of Cascade, a key component of bacteria's sophisticated immune system known as CRISPR, an acronym for Clustered Regularly Interspaced Short Palindromic Repeats. Cascade uses the information housed in sequences of RNA as shorthand to identify foreign invaders and kill them.


Much of the human immune system is well understood, but until recently scientists didn't realize the level of complexity associated with the immune system of single-cell life forms, including bacteria. Scientists first identified CRISPR several years ago when trying to understand why bacterial cultures used to make yogurt succumbed to viral infections. Researchers subsequently discovered they could harness the CRISPR bacterial immune system to edit DNA and repair damaged genes. One group, for example, was able to remove viral DNA from human cells infected with HIV.


Bailey's work is focused on how Cascade is able to help bacteria fight off viruses called bacteriophages. The Cascade system uses short strands of bacterial RNA to scan the bacteriophage DNA to see if it is foreign or self. If foreign, the cell launches an attack that chews up the invading bacteriophage.


To "see" how this happens, Bailey and his team converted Cascade into a crystalized form. Technicians at the National Synchrotron Light Source at Brookhaven National Laboratory in Upton, NY, and the Stanford Synchrotron Radiation Lightsource then trained high-powered X-rays on the crystals. The X-rays provided computational data to the Bloomberg School scientists allowing them to draw Cascade, an 11-protein machine that only operates if each part is in perfect working order.


What they saw was unexpected. Instead of the RNA and DNA wrapping around each other to form what is known as a double-helix structure, in Cascade the DNA and RNA are more like parallel lines, forming something of a ladder. Bailey says that if RNA had to wrap itself around DNA to recognize an invader -- and then unwrap itself to look at the next strand -- the process would take too much time to ward off infection. With a ladder structure, RNA can quickly scan DNA.


In the new study, Bailey says his team determined that the RNA scans the DNA in a manner similar to how humans scan text for a key word. They break long stretches of characters into smaller bite-sized segments, much like words themselves, so they can be spotted more easily.


Since the CRISPR-Cas system naturally acts as a barrier to the exchange of genetic information between bacteria and bacteriophages, its function can offer clues to how antibiotic resistance develops and ideas for how to keep it from happening.


"We're finding more pieces to the puzzle," Bailey says. "This gives us a better understanding of how these machines find their targets, which may help us harness the CRISPR system as a tool for therapy or manipulation of DNA in a lab setting. And it all started when someone wanted to make yogurt more cheaply."


"Crystal structure of a CRISPR RNA-guided surveillance complex bound to a ssDNA target," was written by Sabin Mulepati, Annie Heroux and Scott Bailey.



Hoopoes' eggs show their true colors

Hoopoe females use cosmetics on their eggs -- and the eggs gradually change color when they are incubated, from bluish-grey to a more saturated greenish-brown. This happens because secretion from the uropygial or preen gland -- a substance birds use to preen and protect their feathers -- is transfered from the female hoopoe's gland to her eggs directly with the bill and by means of belly feathers. This is one of the findings from a study led by Juan J. Soler of the Estación Experimental de Zonas Áridas, CSIC in Spain, published in Springer's journal Naturwissenschaften -- The Science of Nature.



Previous work by Soler´s team has shown that the preen gland secretion of incubating hoopoes is brown in color and holds antimicrobial properties. The color is thanks to a combination of symbiotic bacteria found in the uropygial gland that provides protection against pathogenic bacteria. The symbiotic bacteria help to protect embryos from trans-shell infections, and in vitro are highly effective against Bacillus licheniformis, a well-known feather-degrading bacterium. The darker the color of the secretion, the more of the "good" bacteria are present -- and the better protection there is against the "bad" bacteria to ensure that a bird's embryos or feathers stay healthy.


To find out if indeed it is the gland secretion that causes hoopoes' eggs to change color, Soler's team conducted field studies in southern Spain and experimental work at the University of Granada and in Finca Experimental la Hoya in Almeria. In some cases, the researchers blocked off female hoopoes' uropygial glands found over their tails, to make it impossible for them to spread any preen oil onto their feathers or eggs. In other instances, the researchers smeared eggshells with this preen oil.


Their experimental tests showed that eggs that came into contact with the gland secretion changed color from their initial bluish-grey to greenish-brown. Eggs that were not covered with this so-called preen oil showed no color change.


"The eggshell coloration of hoopoe eggs is the consequence of the female birds' spreading uropygial secretion on the eggshells," says Soler.


The researchers speculate that the egg coloration might be a way through which a female hoopoe signals to the male that she is good breeding material, for future reference. It can inform a male of the presence, abundance, or even particularities of the antimicrobial bacterial community found in a female's glands -- qualities that she will be able to carry over to their offspring should they mate in the future. Males can use this information to adjust their investment in the actual breeding attempt. Although further experimental work is needed to establish the validity of this signaling hypothesis, Soler hopes that the new results will encourage such research in hoopoes and in other birds.




Story Source:


The above story is based on materials provided by Springer Science+Business Media . Note: Materials may be edited for content and length.



A 1996 Plan to Use NASA’s Oldest Orbiter to Make Money on the Moon


Columbia_Moon2

NASA



Assembly of NASA’s first spaceworthy Space Shuttle Orbiter, OV-102 Columbia, commenced in March 1975. The 111-ton reusable winged spaceship first reached low-Earth orbit on STS-1 (12-14 April 1981), the Space Shuttle Program’s first mission. Named for the first American sailing ship to circle the globe and the Apollo 11 Command and Service Module, Columbia completed 27 successful flights.

NASA’s oldest Orbiter was also its heaviest. Unlike its sisters Atlantis, Discovery, and Endeavor, Columbia had difficulty reaching the 51.6° orbital inclination of the Russian Mir station and the International Space Station (ISS) with a useful payload in its 15-by-60-foot payload bay. It was the only Orbiter that did not visit the Russian Mir station. This performance constraint meant that, in the Shuttle-Mir/ISS era, NASA relegated to Columbia its few remaining low-inclination, non-space station missions, such as Hubble Space Telescope servicing.


Extended-Duration Orbiter modifications would permit Columbia to remain in orbit for more than two weeks to serve as a science research platform. Such missions would, however, become increasingly rare – or end entirely – as research expanded on board ISS.


In an April 1996 paper presented at the 33rd Space Congress in Cocoa Beach, Florida, Carey McCleskey of the Vehicle Engineering Directorate at NASA’s Kennedy Space Center proposed using the oldest Orbiter’s excess mission capacity “to ignite a billion dollar, sustained enterprise on the Moon.” Specifically, he advocated using Columbia as a joint NASA/private sector Earth-orbital launch platform for rocket stages bearing small lunar landers. Columbia would remain in space for only a few hours during each of its lunar lander deployment missions.


The first Space Shuttle launch: Columbia lifts off at the start of STS-1 on 12 April 1981.

The first Space Shuttle launch: Columbia lifts off at the start of STS-1 on 12 April 1981. NASA



The landers would deliver to the moon teleoperated “micro-robots” akin to Mars Pathfinder’s Sojourner minirover. These would serve as proxy lunar explorers for paying visitors at “space theme parks” on Earth.


Confident that his proposal would help to build public support for U.S. astronauts to return to the moon, McCleskey wrote that



use of Columbia only makes sense for the start-up and initial take-off phases of the enterprise. The Shuttle system. . .will reach a limit which will drive the nation toward advanced space delivery systems. The use of the Shuttle for starting a lunar enterprise, therefore, is not the answer for space delivery, but rather our next opportunity.



Columbia lifted off at the start of STS-107, its 28th mission, on 16 January 2003. Eighty-two seconds after launch, a piece of foam insulation about 20 inches long broke free from its External Tank and struck its left wing. Engineers examining high-resolution video images of the impact warned of possible wing damage, but Shuttle management elected to disregard their warnings.


The oldest Orbiter’s seven-person crew conducted wide-ranging science research for 16 days – long enough for the moon to wax from nearly full to full, then wane to last quarter and new. The crew beamed to Earth a breathtaking image of the last quarter moon taken on 26 January (image at top of post).


On 1 February 2003, the day of the new moon, Columbia fired its twin Orbital Maneuvering System engines to slow itself and reenter Earth’s atmosphere. Temperatures on the Orbiter’s belly tiles, nose cap, and wing leading edge panels began to climb as Columbia reentered at an altitude of 400,000 feet. About 40 minutes after the deorbit burn the wing leading edge temperature neared its peak value of about 3000° Fahrenheit.


As Columbia crossed the California coast in predawn darkness en route to its planned landing in Florida, hot plasma began to penetrate its internal structure through a breach in its left wing leading edge. Flight controllers in Mission Control in Houston puzzled over the cause of sensor failures in the Orbiter’s left wing. The failures progressed aftward from the leading edge.


For observers on the ground in California, Nevada, Utah, Arizona, Colorado, New Mexico, and Texas, many of whom had observed pre-dawn Shuttle reentries before, Columbia was a fast-moving, brilliant point of light leaving behind a luminous, sky-spanning ionization trail. Veteran observers along Columbia‘s reentry path noted more than 20 unusual flashes around the Orbiter and peculiar bright streaks in the trail.


As Columbia crossed from New Mexico into Texas, it began to shed pieces. Meanwhile, thrusters fired automatically to compensate for increased drag on the left wing. Columbia did not give up without a fight.


Radio contact with Columbia was lost about 10 minutes after hot plasma first entered the left wing. Less than a minute later, the gutted wing folded over the fuselage. The oldest Orbiter tumbled and disintegrated at an altitude of 203,000 feet just west of Dallas, Texas, killing its crew and raining wreckage over parts of eastern Texas and western Louisiana.


Had Columbia not been destroyed, NASA would have launched it to the ISS for the first (and probably only) time in November 2003. The STS-118 mission would have seen NASA’s oldest Orbiter stand in for its younger sister Discovery, which was scheduled for periodic maintenance. As it turned out, Endeavour, the Orbiter built to replace Challenger, carried out STS-118 in August 2007. Columbia was the only Orbiter that never visited a space station.


The STS-107 accident triggered far-reaching changes in the U.S. space program that even now have yet to play out fully. Most obvious of these was President George W. Bush’s January 2004 call to end the Space Shuttle Program when ISS was completed, which at the time was scheduled for 2010. The 135th and last flight of the Shuttle, designated STS-135, concluded on 21 July 2011, with the landing of Atlantis in Florida. On 16 August 2011, Space Shuttle Program Manager John Shannon announced that the Shuttle Program would end officially on 31 August 2011.


Reference


“Using the Space Shuttle Columbia to Begin Bringing the Moon to America,” Carey M. McCleskey; paper presented at the 33rd Space Congress in Cocoa Beach, Florida, April 23-26, 1996.


Related Beyond Apollo Posts


Space Station Columbia (1991)


Columbia, Discovery, and Atlantis


Ten Years After Columbia: A List of Shuttle-Station Posts