Saturday, December 22, 2007
'Wall Of Africa' Allowed Humanity To Emerge
Finding: The accelerated uplift of mountains and highlands stretching from Ethiopia to South Africa blocked much ocean moisture, converting lush tropical forests into an arid patchwork of woodlands and savannah grasslands that gradually favored human ancestors who came down from the trees and started walking on two feet -- an energy-efficient way to search larger areas for food in an arid environment.
Scientists long have focused on how climate and vegetation allowed human ancestors to evolve in Africa. Now, University of Utah geologists are calling renewed attention to the idea that ground movements formed mountains and valleys, creating environments that favored the emergence of humanity.
Tectonics
Tectonics or the movement of Earth's crust may have been ultimately responsible for the evolution of humankind. This includes the movements of Earth's crust, its ever-shifting tectonic plates and the creation of mountains, valleys and ocean basins. It also includes the 3,700-mile-long stretch of highlands and mountains also known as "the Wall of Africa." It parallels the East African Rift valley, where many fossils of human ancestors were found.
As a topic about the influence on human evolution tectonics has been discussed since at least 1983. But much of the previous discussion of how climate affected human evolution involves global climate changes, such as those caused by cyclic changes in Earth's orbit around the sun, and not local and regional climate changes caused by East Africa's rising landscape.
However, 0ver the last 7 million years the crustal movement or tectonism in East Africa, the landscape drastically changed. That landscape controlled climate on a local to regional scale. That climate change spurred human ancestors to evolve away from the ape line.
Hominins (the new scientific word for humans (Homo) and their ancestors, including Ardipithecus, Paranthropus and Australopithecus) split from apes on the evolutionary tree roughly 7 million to 4 million years ago. The earliest undisputed hominin was Ardipithecus ramidus 4.4 million years ago. The earliest Homo arose 2.5 million years ago, and our species, Homo sapiens, almost 200,000 years ago.
A Force from within the Earth
The geological or tectonic forces shaping Africa begin deep in the Earth, where a "superplume" of hot and molten rock has swelled upward for at least the past 45 million years. This superplume and its branching smaller plumes help push apart the African and Arabian tectonic plates of Earth's crust, forming the Red Sea, Gulf of Aden and the Great Rift Valley that stretches from Syria to southern Africa.
As part of this process, Africa is being split apart along the East African Rift, a valley bounded by elevated "shoulders" a few tens of miles wide and sitting atop "domes" a few hundreds of miles wide and caused by upward bulging of the plume.
The East African Rift runs about 3,700 miles from the Ethiopian Plateau south-southwest to South Africa's Karoo Plateau. It is up to 370 miles wide and includes mountains reaching a maximum elevation of about 19,340 feet at Mount Kilimanjaro.
The rift "is characterized by volcanic peaks, plateaus, valleys and large basins and freshwater lakes," including sites where many fossils of early humans and their ancestors have been found, says Nahid Gani (pronounced nah-heed go-knee), a research scientist. There was some uplift in East Africa as early as 40 million years ago, but "most of these topographic features developed between 7 million and 2 million years ago."
A Wall Rises and New Species Evolve
The Wall of Africa started to form around 30 million years ago, recent studies show most of the uplift occurred between 7 million and 2 million years ago, just about when hominins split off from African apes, developed bipedalism and evolved bigger brains.
Nature built this wall, and then humans could evolve, walk tall and think big.
Is there any characteristic feature of the Wall that drove human evolution?
The answer is the variable landscape and vegetation resulting from uplift of the Wall of Africa, which created a topographic barrier to moisture, mostly from the Indian Ocean and dried the climate. Contrary to those who cite global climate cycles, the climate changes in East Africa were local and resulted from the uplift of different parts of the wall at different times.
The change from forests to a patchwork of woodland and open savannah did not happen everywhere in East Africa at the same time, and the changes also happened in East Africa later than elsewhere in the world.
The Rise of the Wall
Studies of the roughly 300-mile-by-300-mile Ethiopian Plateau, which is the most prominent part of the Wall of Africa indicated the plateau reached its present average elevation of 8,200 feet 25 million years ago. New analysis shows that the rates at which the Blue Nile River cut down into the Ethiopian Plateau, creating a canyon that rivals North America's Grand Canyon.
The conclusion: There were periods of low-to-moderate incision and uplift between 29 million and 10 million years ago, and again between 10 million and 6 million years ago, but the most rapid uplift of the Ethiopian Plateau (by some 3,200 vertical feet) happened 6 million to 3 million years ago.
Other research has shown the Kenyan part of the wall rose mostly between 7 million and 2 million years ago, mountains in Tanganyika and Malawi were uplifted mainly between 5 million and 2 million years ago, and the wall's southernmost end gained most of its elevation during the past 5 million years.
The Time Frame of the Wall development and Human evolution
Clearly, the Wall of Africa grew to be a prominent elevated feature over the last 7 million years, thereby playing a prominent role in East African aridification by wringing moisture out of monsoonal air moving across the region. That period coincides with evolution of human ancestors in the area.
The earliest undisputed evidence of true bipedalism (as opposed to knuckle-dragging by apes) is 4.1 million years ago in Australopithecus anamensis, but some believe the trait existed as early as 6 million to 7 million years ago.
The shaping of varied landscapes by tectonic forces -- lake basins, valleys, mountains, grasslands, woodlands could also be responsible, at a later stage, for hominins developing a bigger brain as a way to cope with these extremely variable and changing landscapes in which they had to find food and survive predators.
For now the lack of more precise timeframes makes it difficult to link specific tectonic events to the development of upright walking, bigger brains and other key steps in human evolution.
Thursday, December 20, 2007
Evolution With A Restricted Number Of Genes
Finding: RNA polymerase II is highly conserved through evolution, with many of its structural characteristics being conserved between bacteria and humans. The development of higher forms of life would appear to have been influenced by RNA polymerase II. This enzyme transcribes the information coded by genes from DNA into messenger-RNA (mRNA), which in turn is the basis for the production of proteins.
Single-Cell Organisms and the Problem of Complexity
Single-cell organisms were already in existence 500 million years ago, with several thousand genes providing different cellular functions. Further developments seemed dependent on producing even more genes.
It would appear that for a highly developed organism like a human, this form of evolution would have resulted in several million genes. But researchers were surprised to learn, following publication of the human genome, that a human only has around 25,000 genes – not many more than a fruit fly or a worm with approximately 15,000 to 20,000 genes.
It would appear that, over the last 500 million years, other ways to produce highly complex organisms have evolved. Evolution has simply found more efficient ways to use the genes already there. But what could have made this possible?
Is there an answer? Yes - it involves the RNA
New results represent a piece of the puzzle and shed new light on to the purpose of an unusual structure in RNA polymerase II.
They build on earlier observations that gene expression is not just regulated by binding of the enzyme to the gene locus to which it is recruited, but also during the phase of active transcription from DNA into RNA. During this phase, parts of the newly synthesised RNA may be removed and the remaining sequences combined into new RNA message. This ‘splicing’ of RNA occurs during gene transcription, and in extreme cases, can produce RNAs coding for several thousand different proteins from a single gene.
How it Works - The Development of CTD
But what was the development that permitted this advance in gene usage? The RNA polymerase II has developed a structure composed of repeats of a 7 amino-acid sequence. In humans this structure – termed “carboxyterminal domain” or CTD – is composed of 52 such repeats. It is placed exactly at the position where RNA emerges from RNA polymerase II. In less complex organisms the CTD is much shorter: a worm has 36 repeats, and yeast as few as 26, but many single-cell organisms and bacteria have never developed an obvious CTD structure.
Although the requirement of CTD for the expression of cellular genes in higher organisms is undisputed, the molecular details for the gene-specific maturation of RNAs is still largely enigmatic. Research groups have now shown a differential requirement for phosphorylation of the amino acid serine at position 7 of CTD in the processing and maturation of specific gene products.
These results provide the groundwork for the discovery of further pieces of the CTD puzzle and thus enlarge our knowledge of gene regulation. Given its fundamental importance, understanding the mechanism of gene regulation is essential if we are to understand cancer and other diseases at the molecular level and develop new therapies.
Single-Cell Organisms and the Problem of Complexity
Single-cell organisms were already in existence 500 million years ago, with several thousand genes providing different cellular functions. Further developments seemed dependent on producing even more genes.
It would appear that for a highly developed organism like a human, this form of evolution would have resulted in several million genes. But researchers were surprised to learn, following publication of the human genome, that a human only has around 25,000 genes – not many more than a fruit fly or a worm with approximately 15,000 to 20,000 genes.
It would appear that, over the last 500 million years, other ways to produce highly complex organisms have evolved. Evolution has simply found more efficient ways to use the genes already there. But what could have made this possible?
Is there an answer? Yes - it involves the RNA
New results represent a piece of the puzzle and shed new light on to the purpose of an unusual structure in RNA polymerase II.
They build on earlier observations that gene expression is not just regulated by binding of the enzyme to the gene locus to which it is recruited, but also during the phase of active transcription from DNA into RNA. During this phase, parts of the newly synthesised RNA may be removed and the remaining sequences combined into new RNA message. This ‘splicing’ of RNA occurs during gene transcription, and in extreme cases, can produce RNAs coding for several thousand different proteins from a single gene.
How it Works - The Development of CTD
But what was the development that permitted this advance in gene usage? The RNA polymerase II has developed a structure composed of repeats of a 7 amino-acid sequence. In humans this structure – termed “carboxyterminal domain” or CTD – is composed of 52 such repeats. It is placed exactly at the position where RNA emerges from RNA polymerase II. In less complex organisms the CTD is much shorter: a worm has 36 repeats, and yeast as few as 26, but many single-cell organisms and bacteria have never developed an obvious CTD structure.
Although the requirement of CTD for the expression of cellular genes in higher organisms is undisputed, the molecular details for the gene-specific maturation of RNAs is still largely enigmatic. Research groups have now shown a differential requirement for phosphorylation of the amino acid serine at position 7 of CTD in the processing and maturation of specific gene products.
These results provide the groundwork for the discovery of further pieces of the CTD puzzle and thus enlarge our knowledge of gene regulation. Given its fundamental importance, understanding the mechanism of gene regulation is essential if we are to understand cancer and other diseases at the molecular level and develop new therapies.
Tuesday, December 18, 2007
Losses Of Long-established Genes Contribute To Human Evolution
Finding: While it is well understood that the evolution of new genes leads to adaptations that help species survive, gene loss may also afford a selective advantage. A group of scientists has investigated this less-studied idea, carrying out the first systematic computational analysis to identify long-established genes that have been lost across millions of years of evolution leading to the human species.
The idea that gene losses might contribute to adaptation has been kicked around, but not well studied.
To find gene losses a software program called TransMap. The program compared the mouse and human genomes, searching for genes having changes significant enough to render them nonfunctional somewhere during the 75 million years since the divergence of the mouse and the human.
Genes can be lost in many ways. This study focused on losses caused by mutations that disrupt the open reading frame (ORF-disrupting mutations). These are either point mutations, where events such as the insertion or substitution of a DNA base alter the instructions delivered by the DNA, or changes that occur when a large portion of a gene is deleted altogether or moves to a new place on the genome.
Using the Dog Genome
The dog genome was used as an out-group to filter out false positives because the dog diverged from our ancient common ancestor earlier than the mouse. So if a gene is still living in both dog and mouse but not in human, it was probably living in the common ancestor and then lost in the human lineage.
Using this process, they identified 26 losses of long-established genes, including 16 that were not previously known.
The gene loss candidates found in the study do not represent a complete list of gene losses of long-established genes in the human lineage, because the analysis was designed to produce more false negatives than false positives.
The study compares multiple genomes
Next they compared the identified genes in the complete genomes of the human, chimpanzee, rhesus monkey, mouse, rat, dog, and opossum to estimate the amount of time the gene was functional before it was lost. This refined the timing of the gene loss and also served as a benchmark for whether the gene in question was long-established, and therefore probably functional, or merely a loss of a redundant gene copy. Through this process, they found 6 genes that were lost only in the human.
The ACYL3 Protein - A loss From many to none
One previously unknown loss, the gene for acyltransferase-3 (ACYL3), was particularly important. This is an ancient protein that exists throughout the whole tree of life. Multiple copies of the ACYL3 gene are encoded in the fly and worm genomes. In the mammalian clade there is only one copy left, and somewhere along primate evolution, that one copy was lost to the primate clan.
Next it was found that this gene contains a nonsense mutation in both human and chimp, and it appears to still look functional in rhesus. Further, they found that the mutation is not present in the orangutan, so the gene is probably still functional in that species. On the evolutionary tree leading to human, on the branch between chimp and orangutan sits gorilla. Knowing if the gene was still active in gorilla would narrow down the timing of the loss.
The gorilla DNA sequence showed the gene intact, without the mutation, so the loss likely occurred between the speciation of gorilla and chimpanzee.
Other Functional Losses
Acyltransferase-3 was not the only lost gene that doesn't have any close functional homologues in the human genome. A highlight of the research was that they were able to find a list of these orphan losses. Some of them have been functional for more than 300 million years, and they were the last copies left in the human genome. While the copies of these genes remaining in the human genome appear to be nonfunctional, functional copies of all of them exist in the mouse genome.
These orphan genes may be interesting candidates for experimental biologists to explore. It will be interesting to find out what was the biological effect of these losses. Once their function is well characterized in species that still have active copies, we could maybe speculate about their effects on human evolution.
The idea that gene losses might contribute to adaptation has been kicked around, but not well studied.
To find gene losses a software program called TransMap. The program compared the mouse and human genomes, searching for genes having changes significant enough to render them nonfunctional somewhere during the 75 million years since the divergence of the mouse and the human.
Genes can be lost in many ways. This study focused on losses caused by mutations that disrupt the open reading frame (ORF-disrupting mutations). These are either point mutations, where events such as the insertion or substitution of a DNA base alter the instructions delivered by the DNA, or changes that occur when a large portion of a gene is deleted altogether or moves to a new place on the genome.
Using the Dog Genome
The dog genome was used as an out-group to filter out false positives because the dog diverged from our ancient common ancestor earlier than the mouse. So if a gene is still living in both dog and mouse but not in human, it was probably living in the common ancestor and then lost in the human lineage.
Using this process, they identified 26 losses of long-established genes, including 16 that were not previously known.
The gene loss candidates found in the study do not represent a complete list of gene losses of long-established genes in the human lineage, because the analysis was designed to produce more false negatives than false positives.
The study compares multiple genomes
Next they compared the identified genes in the complete genomes of the human, chimpanzee, rhesus monkey, mouse, rat, dog, and opossum to estimate the amount of time the gene was functional before it was lost. This refined the timing of the gene loss and also served as a benchmark for whether the gene in question was long-established, and therefore probably functional, or merely a loss of a redundant gene copy. Through this process, they found 6 genes that were lost only in the human.
The ACYL3 Protein - A loss From many to none
One previously unknown loss, the gene for acyltransferase-3 (ACYL3), was particularly important. This is an ancient protein that exists throughout the whole tree of life. Multiple copies of the ACYL3 gene are encoded in the fly and worm genomes. In the mammalian clade there is only one copy left, and somewhere along primate evolution, that one copy was lost to the primate clan.
Next it was found that this gene contains a nonsense mutation in both human and chimp, and it appears to still look functional in rhesus. Further, they found that the mutation is not present in the orangutan, so the gene is probably still functional in that species. On the evolutionary tree leading to human, on the branch between chimp and orangutan sits gorilla. Knowing if the gene was still active in gorilla would narrow down the timing of the loss.
The gorilla DNA sequence showed the gene intact, without the mutation, so the loss likely occurred between the speciation of gorilla and chimpanzee.
Other Functional Losses
Acyltransferase-3 was not the only lost gene that doesn't have any close functional homologues in the human genome. A highlight of the research was that they were able to find a list of these orphan losses. Some of them have been functional for more than 300 million years, and they were the last copies left in the human genome. While the copies of these genes remaining in the human genome appear to be nonfunctional, functional copies of all of them exist in the mouse genome.
These orphan genes may be interesting candidates for experimental biologists to explore. It will be interesting to find out what was the biological effect of these losses. Once their function is well characterized in species that still have active copies, we could maybe speculate about their effects on human evolution.
Wednesday, December 12, 2007
Human Ancestors More Primitive That Once Thought
Finding: A team of researchers has determined through analysis of the earliest known hominid fossils outside of Africa, recently discovered in Dmanisi, Georgia, that the first human ancestors to inhabit Eurasia were more primitive than previously thought.
The fossils, dated to 1.8 million years old, show some modern aspects of lower limb morphology, such as long legs and an arched foot, but retain some primitive aspects of morphology in the shoulder and foot. The species had a small stature and brain size more similar to earlier species found in Africa.
The earliest known hominins to have lived outside Africa in temperate zones of Eurasia did not yet display the full set of derived skeletal features the researchers conclude.
What this means
The new evidence shows how this species had the anatomical and behavioral capacity to be successful across a range of environments and expand out of Africa.
This research shows that the limb proportions and behavioral flexibility which allowed this species to expand out of Africa were there at least 1.8 million years ago.
Dmanisi is the site of a medieval village located about 53 miles southwest of Tbilisi, Georgia on a promontory at the confluence of the Mashavera and Phinezauri rivers.
The fossils, dated to 1.8 million years old, show some modern aspects of lower limb morphology, such as long legs and an arched foot, but retain some primitive aspects of morphology in the shoulder and foot. The species had a small stature and brain size more similar to earlier species found in Africa.
The earliest known hominins to have lived outside Africa in temperate zones of Eurasia did not yet display the full set of derived skeletal features the researchers conclude.
What this means
The new evidence shows how this species had the anatomical and behavioral capacity to be successful across a range of environments and expand out of Africa.
This research shows that the limb proportions and behavioral flexibility which allowed this species to expand out of Africa were there at least 1.8 million years ago.
Dmanisi is the site of a medieval village located about 53 miles southwest of Tbilisi, Georgia on a promontory at the confluence of the Mashavera and Phinezauri rivers.
Monday, December 10, 2007
New Insights Into The Evolution Of The Human Genome
Which came first, the chicken genome or the egg genome?
Genomes have an ability to copy a long stretch of DNA from one chromosome and insert it into another region of the genome. Segmental duplications hold many evolutionary secrets and uncovering them is a difficult biological and computational challenge with implications for both medicine and our understanding of evolution.
Evolutionary History
Researchers have created the first evolutionary history of the duplications in the human genome that are partly responsible for both disease and recent genetic innovations. This marks an important step toward a better understanding of what genomic changes paved the way for modern humans, when these duplications occurred and what the associated costs are - in terms of susceptibility to disease-causing genetic mutations.
In the past, the highly complex patterns of DNA duplication -- including duplications within duplications -- have prevented the construction of an evolutionary history of these long DNA duplications. To crack the duplication code and determine which of the DNA segments are originals (ancestral duplications) and which are copies (derivative duplications), the researchers looked to both algorithmic biology and comparative genomics.
Identifying the original duplications is a prerequisite to understanding what makes the human genome unstable. Researchers modified an algorithmic genome assembly technique in order to deconstruct the sequence of repeated stretches of DNA and identify the original sequences. The belief is that perhaps there may be something special about the originals, some clue or insight into what causes this colonization of the human genome.
This is the first time that we have a global view of the evolutionary origin of some of the most complicated regions of the human genome. The researchers tracked down the ancestral origin of more than two thirds of these long DNA duplications.
Special Findings:
First, researchers suggest that specific regions of the human genome experienced elevated rates of duplication activity at different times in our recent genomic history. This contrasts with most models of genomic duplication which suggest a continuous model for recent duplications. Second, a large fraction of the recent duplication architecture centers around a rather small subset of "core duplicons" -- short segments of DNA that come together to form segmental duplications. These cores are focal points of human gene/transcript innovations.
Not all of the duplications in the human genome are created equal. Some of them -- the core duplicons -- appear to be responsible for recent genetic innovations the in human genome. Researchers uncovered 14 such core duplicons.
In 4 of the 14 cases, there is compelling evidence that genes embedded within the cores are associated with novel human gene innovations. In two cases the core duplicon has been part of novel fusion genes whose functions appear to be radically different from their antecedents.
Results suggest that the high rate of disease caused by these duplications in the normal population may be offset by the emergence of newly minted human/great-ape specific genes embedded within the duplications. The next challenge will be determining the function of these novel genes.
Mathematical Algorithms and Biological construction
Research applied their expertise in assembling genomes from millions of small fragments -- a problem that is not unlike the "mosaic decomposition" problem in analyzing duplications that the team faced.
Over the years researchers applied the 250-year old algorithmic idea first proposed by 18th century mathematician Leonhard Euler (of the fame of pi) to a variety of problems and demonstrated that it works equally well for a set of seemingly unrelated biological problems including DNA fragment assembly, reconstructing snake venoms, and now dissecting the mosaic structure of segmental duplications.
Finding: The answers provide the first evolutionary history of the duplications in the human genome that are partly responsible for both disease and recent genetic innovations.
This work marks a significant step toward a better understanding of what genomic changes paved the way for modern humans, when these duplications occurred and what the associated costs are -- in terms of susceptibility to disease-causing genetic mutations.
Researchers have answered a similar vexing genomic question: Which of the thousands of long stretches of repeated DNA in the human genome came first? And which are the duplicates?
Genomes have an ability to copy a long stretch of DNA from one chromosome and insert it into another region of the genome. Segmental duplications hold many evolutionary secrets and uncovering them is a difficult biological and computational challenge with implications for both medicine and our understanding of evolution.
Evolutionary History
Researchers have created the first evolutionary history of the duplications in the human genome that are partly responsible for both disease and recent genetic innovations. This marks an important step toward a better understanding of what genomic changes paved the way for modern humans, when these duplications occurred and what the associated costs are - in terms of susceptibility to disease-causing genetic mutations.
In the past, the highly complex patterns of DNA duplication -- including duplications within duplications -- have prevented the construction of an evolutionary history of these long DNA duplications. To crack the duplication code and determine which of the DNA segments are originals (ancestral duplications) and which are copies (derivative duplications), the researchers looked to both algorithmic biology and comparative genomics.
Identifying the original duplications is a prerequisite to understanding what makes the human genome unstable. Researchers modified an algorithmic genome assembly technique in order to deconstruct the sequence of repeated stretches of DNA and identify the original sequences. The belief is that perhaps there may be something special about the originals, some clue or insight into what causes this colonization of the human genome.
This is the first time that we have a global view of the evolutionary origin of some of the most complicated regions of the human genome. The researchers tracked down the ancestral origin of more than two thirds of these long DNA duplications.
Special Findings:
First, researchers suggest that specific regions of the human genome experienced elevated rates of duplication activity at different times in our recent genomic history. This contrasts with most models of genomic duplication which suggest a continuous model for recent duplications. Second, a large fraction of the recent duplication architecture centers around a rather small subset of "core duplicons" -- short segments of DNA that come together to form segmental duplications. These cores are focal points of human gene/transcript innovations.
Not all of the duplications in the human genome are created equal. Some of them -- the core duplicons -- appear to be responsible for recent genetic innovations the in human genome. Researchers uncovered 14 such core duplicons.
In 4 of the 14 cases, there is compelling evidence that genes embedded within the cores are associated with novel human gene innovations. In two cases the core duplicon has been part of novel fusion genes whose functions appear to be radically different from their antecedents.
Results suggest that the high rate of disease caused by these duplications in the normal population may be offset by the emergence of newly minted human/great-ape specific genes embedded within the duplications. The next challenge will be determining the function of these novel genes.
Mathematical Algorithms and Biological construction
Research applied their expertise in assembling genomes from millions of small fragments -- a problem that is not unlike the "mosaic decomposition" problem in analyzing duplications that the team faced.
Over the years researchers applied the 250-year old algorithmic idea first proposed by 18th century mathematician Leonhard Euler (of the fame of pi) to a variety of problems and demonstrated that it works equally well for a set of seemingly unrelated biological problems including DNA fragment assembly, reconstructing snake venoms, and now dissecting the mosaic structure of segmental duplications.
Monday, November 26, 2007
DNA is a vestige of formation of liquid crystal order
Finding: Scientists have discovered liquid crystals of ultrashort DNA molecules immersed in water, providing a new scenario for a key step in the emergence of life on Earth.
The research team found that surprisingly short segments of DNA, life's molecular carrier of genetic information, could assemble into several distinct liquid crystal phases that "self-orient" parallel to one another and stack into columns when placed in a water solution.
Life is widely believed to have emerged as segments of DNA- or RNA-like molecules in a prebiotic "soup" solution of ancient organic molecules.
The conventional View Random formation of DNA is not possible.
If the formation of molecular chains as uniform as DNA by random chemistry is essentially impossible, then what are the effective ways for simple molecules to spontaneously self-select, "chain-up" and self-replicate.
What the study shows
In a mixture of tiny fragments of DNA, those molecules capable of forming liquid crystals selectively condense into droplets in which conditions are favorable for them to be chemically linked into longer molecules with enhanced liquid crystal-forming tendencies.
Even tiny fragments of double helix DNA can spontaneously self-assemble into columns that contain many molecules. From the collection of ancient molecules, short RNA pieces or some structurally related precursor emerged as the molecular fragments most capable of condensing into liquid crystal droplets, selectively developing into long molecules.
What are Liquid Crystals?
Liquid crystals are organic materials related to soap that exhibit both solid and liquid properties. They are commonly used for information displays in computers, flat-panel televisions, cell phones, calculators and watches.
What affects liquid crystals?
Most liquid crystal phase molecules are rod-shaped and have the ability to spontaneously form large domains of a common orientation, which makes them particularly sensitive to stimuli like changes in temperature or applied voltage.
RNA and DNA are chain-like polymers with side groups known as nucleotides, or bases, that selectively adhere only to specific bases on a second chain. Matching, or complementary base sequences enable the chains to pair up and form the widely recognized double helix structure. Genetic information is encoded in sequences of thousands to millions of bases along the chains, which can be microns to millimeters in length.
Such DNA polynucleotides had previously been shown to organize into liquid crystal phases in which the chains spontaneously oriented parallel to each other. Researchers understand the liquid crystal organization to be a result of DNA's elongated molecular shape, making parallel alignment easier, much like spaghetti thrown in a box and shaken would be prone to line up in parallel.
How short is short?
A series of experiments were conducted to see how short the DNA segments could be and still show liquid crystal ordering. The team found that even a DNA segment as short as six bases, when paired with a complementary segment that together measured just two nanometers long and two nanometers in diameter, could still assemble itself into the liquid crystal phases, in spite of having almost no elongation in shape.
What does this mean?
Structural analysis of the liquid crystal phases showed that they appeared because such short DNA duplex pairs were able to stick together "end-to-end," forming rod-shaped aggregates that could then behave like much longer segments of DNA. The sticking was a result of small, oily patches found on the ends of the short DNA segments that help them adhere to each other in a reversible way -- much like magnetic buttons -- as they expelled water in between them.
Columnar Stacking is possible if the nanoDna can form duplexes
The experiments provided direct evidence for the columnar stacking of the nano DNA pieces in a fluid liquid crystal phase. The key observation with respect to early life is that this aggregation of nano DNA strands is possible only if they form duplexes. In a sample of chains in which the bases don't match and the chains can't form helical duplexes, we did not observe liquid crystal ordering.
Complementary and noncomplementary DNA segments
Additional tests by the team involved mixed solutions of complementary and noncomplementary DNA segments. The results indicated that essentially all of the complementary DNA bits condensed out in the form of liquid crystal droplets, physically separating them from the noncomplementary DNA segments.
Significance for DNA molecules
The significance is that small molecules with the ability to pair up the right way can seek each other out and collect together into drops that are internally self-organized to facilitate the growth of larger pairable molecules.
DNA is a vestige of formation of liquid crystal order
The liquid crystal phase condensation selects the appropriate molecular components, and with the right chemistry would evolve larger molecules tuned to stabilize the liquid crystal phase. If this is correct, the linear polymer shape of DNA itself is a vestige of formation by liquid crystal order.
The research team found that surprisingly short segments of DNA, life's molecular carrier of genetic information, could assemble into several distinct liquid crystal phases that "self-orient" parallel to one another and stack into columns when placed in a water solution.
Life is widely believed to have emerged as segments of DNA- or RNA-like molecules in a prebiotic "soup" solution of ancient organic molecules.
The conventional View Random formation of DNA is not possible.
If the formation of molecular chains as uniform as DNA by random chemistry is essentially impossible, then what are the effective ways for simple molecules to spontaneously self-select, "chain-up" and self-replicate.
What the study shows
In a mixture of tiny fragments of DNA, those molecules capable of forming liquid crystals selectively condense into droplets in which conditions are favorable for them to be chemically linked into longer molecules with enhanced liquid crystal-forming tendencies.
Even tiny fragments of double helix DNA can spontaneously self-assemble into columns that contain many molecules. From the collection of ancient molecules, short RNA pieces or some structurally related precursor emerged as the molecular fragments most capable of condensing into liquid crystal droplets, selectively developing into long molecules.
What are Liquid Crystals?
Liquid crystals are organic materials related to soap that exhibit both solid and liquid properties. They are commonly used for information displays in computers, flat-panel televisions, cell phones, calculators and watches.
What affects liquid crystals?
Most liquid crystal phase molecules are rod-shaped and have the ability to spontaneously form large domains of a common orientation, which makes them particularly sensitive to stimuli like changes in temperature or applied voltage.
RNA and DNA are chain-like polymers with side groups known as nucleotides, or bases, that selectively adhere only to specific bases on a second chain. Matching, or complementary base sequences enable the chains to pair up and form the widely recognized double helix structure. Genetic information is encoded in sequences of thousands to millions of bases along the chains, which can be microns to millimeters in length.
Such DNA polynucleotides had previously been shown to organize into liquid crystal phases in which the chains spontaneously oriented parallel to each other. Researchers understand the liquid crystal organization to be a result of DNA's elongated molecular shape, making parallel alignment easier, much like spaghetti thrown in a box and shaken would be prone to line up in parallel.
How short is short?
A series of experiments were conducted to see how short the DNA segments could be and still show liquid crystal ordering. The team found that even a DNA segment as short as six bases, when paired with a complementary segment that together measured just two nanometers long and two nanometers in diameter, could still assemble itself into the liquid crystal phases, in spite of having almost no elongation in shape.
What does this mean?
Structural analysis of the liquid crystal phases showed that they appeared because such short DNA duplex pairs were able to stick together "end-to-end," forming rod-shaped aggregates that could then behave like much longer segments of DNA. The sticking was a result of small, oily patches found on the ends of the short DNA segments that help them adhere to each other in a reversible way -- much like magnetic buttons -- as they expelled water in between them.
Columnar Stacking is possible if the nanoDna can form duplexes
The experiments provided direct evidence for the columnar stacking of the nano DNA pieces in a fluid liquid crystal phase. The key observation with respect to early life is that this aggregation of nano DNA strands is possible only if they form duplexes. In a sample of chains in which the bases don't match and the chains can't form helical duplexes, we did not observe liquid crystal ordering.
Complementary and noncomplementary DNA segments
Additional tests by the team involved mixed solutions of complementary and noncomplementary DNA segments. The results indicated that essentially all of the complementary DNA bits condensed out in the form of liquid crystal droplets, physically separating them from the noncomplementary DNA segments.
Significance for DNA molecules
The significance is that small molecules with the ability to pair up the right way can seek each other out and collect together into drops that are internally self-organized to facilitate the growth of larger pairable molecules.
DNA is a vestige of formation of liquid crystal order
The liquid crystal phase condensation selects the appropriate molecular components, and with the right chemistry would evolve larger molecules tuned to stabilize the liquid crystal phase. If this is correct, the linear polymer shape of DNA itself is a vestige of formation by liquid crystal order.
Saturday, November 24, 2007
Environmental Setting Of Human Migrations In The Circum-Pacific Region
Finding: The expansion of modern human populations into the circum-Pacific region occurred in at least four pulses, in part controlled by climate and sea level changes in the Late Pleistocene and Holocene epochs. Modern humans migrated into eastern Asia via a southern coastal route.A new study adds insight into the migration of anatomically modern humans out of Africa and into Asia less than 100,000 years before present (BP).
Phase 1 45,000 to 40,000 BP Stable climate and sea level
The initial "out of Africa" migration was thwarted by dramatic changes in both sea level and climate and extreme drought in the coastal zone. A period of stable climate and sea level 45,000-40,000 years BP gave rise to the first major pulse of migration, when modern humans spread from India, throughout much of coastal southeast Asia, Australia, and Melanesia, extending northward to eastern Russia and Japan by 37,000 years BP.
33,000 to 16,000 BP Climate change - sea level and cold climate change
The northward push of modern humans along the eastern coast of Asia stalled north of 43° N latitude, probably due to the inability of the populations to adjust to cold waters and tundra/steppe vegetation.
The northward push of modern humans along the eastern coast of Asia stalled north of 43° N latitude, probably due to the inability of the populations to adjust to cold waters and tundra/steppe vegetation.
The ensuing cold and dry Last Glacial period, ~33,000-16,000 year BP, once again brought dramatic changes in sea level and climate, which caused abandonment of many coastal sites.
Phase 2 16,000 to 8,000 BP Climate Warming
After 16,000 years BP, climates began to warm, but sea level was still 100 m below modern levels, creating conditions amenable for a second pulse of human migration into North America across an ice-free coastal plain now covered by the Bering Sea.
Phase 3 8,000 to 6,000 BP climate stabilization
The stabilization of climate and sea level in the early Holocene (8,000-6,000 years BP) supported the expansion of coastal wetlands, lagoons, and coral reefs, which in turn gave rise to a third pulse of coastal settlement, filling in most of the circum-Pacific region.
A drop in sea level in the western Pacific in the mid-Holocene (~6,000-4,000 year BP), caused a reduction in productive coastal habitats, leading to a brief disruption in human subsistence along the then densely settled coast.
Phase 4 3,500 to 1,000 BP
This disruption may have helped initiate the last major pulse of human migration in the circum-Pacific region, that of the migration to Oceania, which began about 3,500 years BP and culminated in the settlement of Hawaii and Easter Island by 2000-1000 years BP.
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