Let There Be Life

How did Earth become biological?

By | March 1, 2014

ANDRZEJ KRAUZEMost cultures have creation myths looking back to a time before life existed, assuaging a universal longing to know from whence we and our world came.

Will scientists ever be able to write a complete origin-of-life story, one based on incontrovertible facts? The opening chapter would require a journey way back in time to when Earth formed some 4.5 billion years ago, oxygenless, pocked with spewing volcanoes, bombarded with asteroids. Yet, somehow life appeared on this planet. Chemistry begat biology. Cells formed from a soup of simple molecules. By 3.5 billion years ago, microbes, perhaps similar to contemporary organisms, existed on Earth. How did that happen? How fast? And where?

A host of researchers from myriad disciplines—geologists, microbiologists, geneticists, astrobiologists, computational biologists, biochemists, and synthetic biologists—are adding fascinating details to the story. This issue of The Scientist offers a glimpse of some of the most current origin-of-life science, from new research on how RNA may have been assembled from precursor molecules to what we now know about our last universal common ancestor.

When Stanley Miller famously isolated a few amino acids from his lab-concocted prebiotic soup, his University of Chicago advisor, Nobel laureate Harold Urey, reportedly remarked, “If God didn’t do it this way, he missed a good bet.” Sixty years later, biochemists are mixing all sorts of simple molecular ingredients presumed to have existed on a prebiotic Earth, with the aim of cooking up the nucleotide monomers of information-bearing molecules that could evolve and give rise to the first proto-cells. In “RNA World 2.0,” Senior Editor Jef Akst lays out the most recent research on how RNA could have formed from a “dirty” mixture that also contained amino acids and fatty acids, and how these early molecules may have cooperated to lead to the cell-based life we see today.

Three articles in the issue illustrate the power of using gene sequences to unlock the history of life on Earth. “Discovering Archaea, 1977” recounts how Carl Woese rocked the foundations of evolutionary biology by using ribosomal RNA (rRNA) sequences to construct a new phylogenetic tree of life with three, rather than two, domains: bacteria, eukaryotes, and archaea. Interestingly, his onetime postdoc and 1977 coauthor of the seminal paper, George Fox, wonders if Woese might have failed to recognize archaea as a new domain had they used modern sequencing techniques instead of gel electrophoresis.

More-recent discoveries of giant viruses with massive genomes have the potential to shake up evolutionary biology once again. Truly giant viruses, with bigger genomes than many bacteria and archaea, escaped detection for decades because microbiologists defined viruses, in part, by their ability to pass through filters with pores 0.2 μm in diameter. Didier Raoult (“Viruses Reconsidered”) describes the discovery of these megaviruses (0.4 μm) that, among other surprises, contain genes encoding the translational machinery for their rep­lication. Woese added archaea to the tree of life based on rRNA sequencing. Viruses have no rRNA, and most biologists do not consider them to be living organisms. But Raoult argues that phylogenetic trees based on transfer RNA and RNA polymerase genes “show that viruses are at least as old as the three traditional domains proposed by Woese” and may warrant classification as a fourth branch of life.

Sitting at the base of the three-domain tree is our last universal common ancestor (LUCA). What researchers can say today about the makeup of LUCA is a direct result of the availability of gene sequences from so many species. Aaron Goldman writes that “LUCA is not [Darwin’s] ‘primordial form,’ but rather a sophisticated cellular organism that, if alive today, would probably be difficult to distinguish from other extant bacteria or archaea.”

So, the scientific origin-of-life story is a biography still unfolding, not yet ready to publish in full. But learning how researchers are filling its pages is nothing short of spellbinding.

Mary Beth Aberlin  Editor-in-Chief  eic@the-scientist.com

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Avatar of: James V. Kohl

James V. Kohl

Posts: 436

March 3, 2014

Does the representation of cause and effect below tell the current tale of what is known about differences in the antigenic properties of viruses?


One or two amino acid substitutions enable the ecological adaptation of avian influenza A viruses, which allow them to infect mammals. One amino acid makes the avian H5N1 virus more lethal to mice.

In the infected cells of mammals, ecological adaptations in the influenza virus appear to be glucose-dependent. Enzymatic inhibition of glycolysis reduces influenza infection.

In the context of protein biophysics and glucose-dependent intracellular and intermolecular signaling, antigenically neutral mutations may accumulate, but glucose-dependent biophysical constraints on protein folding prevent fixation of deleterious mutations in the virus. Epistasis arises in the context of glucose-dependent amino acid substitutions that stabilize the thermodynamics of protein folding in the virus.

It is not fixed mutations, which would perturb the thermodynamic stability of the virus, but it is the amino acid substitutions that result in predictable changes in the antigenic properties of the human influenza virus.

Although glycolysis may not appear to be directly involved in protein biophysics, glucose-dependent amino acid substitutions cause slight variations in strains of the human influenza virus from year to year. These variations result from nutrient-dependent amino acid substitutions, but the variations are typically reported outside the context of what is known about how viruses responds to ecological variation in the availability of glucose.

No experimental evidence suggests beneficial mutations could be fixed in viruses, but amino acid substitutions are reported as if they were mutations that caused changes in the antigenic properties of viruses that somehow benefit the virus. Experimental evidence shows that ecological variation and nutrient-dependent antigenic phenotypes, not genotypes, determine the degree of strain cross-immunity in the human influenza virus. Seasonal influenza typically escapes immunity from vaccines with as little as one amino acid substitution.

Antigenic evolution could be and probably should be correctly reported as nutrient-dependent epigenetically-effected ecological adaptations manifested in deletion of a single amino acid in the haemagglutinin gene of  H1N1 influenza A viruses. Correctly reporting cause and effect in the ecological adaptations of viruses could lead to better preventative measures and treatments of influenza and other viral infections. The old adage, "feed a cold; starve a fever" could be revised. Starve a virus-induced fever might be easier to remember and that might help to prevent ecological adaptations that benefit viruses but not people.

Avatar of: jeenious


Posts: 45

Replied to a comment from James V. Kohl made on March 3, 2014

March 4, 2014








Given the many differences in ways the same sub-sequences of RNA/DNA can participate in providing various species characteristics, to speak of whether a particular sequence, per se, is beneficial to the one and THEREFORE deleterious to the other is meaningless.  What a given portion of a sequence "does" in one species is seldom exactly what its "does" in another.  Not only are there symbiotic relationships between organisms of various sized and kinds but, also, there may be completely dissimilar dynamics using the same sequences . So to compare a particular sequence, in the context of how it is utilized (so to speak) in the DNA of one species, as thout it therefore were deleterious to another comparable to comparing of soup to nuts. 

Many mathematical models demonstrate how a variety of constellations, though  all composed of a limited set of factors, can provide advantage or disadvantage depending upon local context inside a larger context.

In the game of bridge, for example, whether one has a "good hand" can be contingent on how ALL THE OTHER cards are distributed among the other players.  Even so, biologically speaking, what might otherwise be a viable set of characteristics of a species can depend upon the extent to which those same characteristics and other characteristics are distributed among the other flora and fauna in its environment.  And the hand that would be a great hand in a bridge game might get you shot in a poker game for having too many cards.  (If a worm can have more genes than a human, what does that say about additional genes providing additional solutions to coping needs and coming up with something "superior" by human standards?  (: > )... but trying to be serious here...

It is hard to say that the way a particular sequence is expressed in a bacterium and also, say, in a human, yields a distinct advantage to the one as offset by a distince disadvantage in the other.


Not only does the question arise of what a given segment of DNA "does" at various relative size scales (after all, at one size scale, a bacterium, a virus, a human... are made up of quanta of matter and/or energy, where one dynamic applies.  At the genetic level (including different numbers of copies of any given gene sequence) the "work performed" in one species may have to do with one function and in another species another function.  What is "expressed" as a result of the same sequence may be vital, or merely innocuous, in another, and in yet another be deleterious.


Thought it be an over-simplification, the viability of a house rests upon a plethora of materials, hooked together in a plethora of ways, in a plethora of sequences, and in any one of a plethora of different designs.  Thus, although a brick house may require mortar, a wooden house may not.  And, just because two houses are made with bricks and mortar a part of their construction, that does not mean that the two houses have well-ordered floor plans. 


At every level of scale, and at every stage in the process of fertilization, incubation, hatching/birth, growth and development to maturity, procreation, whether or not there is a successful availance of the dynamics applying to that scale can determine whether even the best possible mix of materials and designs and methods of assembly and function at other scales are "good" or "bad."


At the cellular level there could not be any health without apoptosis.


It can be argued, however, that at, say, the human species interaction level (social level) the equivalent of apoptosis does not occur such that deleteriouly peforming (or counter-performing) individuals are efficient in how they induce their own apoptosis, or are caused by other "players" to do so... (and the key word in that sentence is "efficient).


It can be reasonably argued that if we humans were to "solve" all our problems relating to aging and illness and fitness, we would have to stop reproducing entirely, lest we rapidly increase in population to a point at which we would all starve.  And if we used our science then to solve all problems relating to providing all the food our increasing population could ever need, even figuring out a way to avoid depleting Earth's ability to keep the chow coming, our population would then grow unchecked until SOMETHING  ELSE would have to give.  We would surely face the challenge of how to avoid drowning or suffocating in our own collective species excrement... as do yeast cells in a brewing vat, when they have produced so much alcohol they cannot live in it.


But, let's say, we resolve that problem by finding ways to turn our excrement in to food, which takes care of the food supply problem and the excrement problem, and with no horrid side effects. 


Then our population would be disease free, immortal, highly efficient in  reproducing... and we would have no problem with our human or industrial excretions...


But wait!  What would we do with all the newly-born people?


Would our older generations walk on the heads of the new-borns, crushing them?  Or would we put the new-borns on our shoulders upon running out of standing room only, and thence be crushed under their weight?


In either case, let's assume we SOLVE  THAT  PROBLEM, TOO.  How?  Well, by mutating so as to produce smaller and smaller offspring in future generations.  That would enable us to have as much space as we need... up to the kinds of limits that only bacteria and viruses need worry about.


Of course, at some point in that ever-smaller-sizes of offspring, we would run into the problem of having to give up our large brain size, and become less intelligent than we are. 


But perhaps a surprise solution would come to the PROBLEM of science solving all our problems.  It would be a self-curing proglem.  Without these big brains, and our sciences enabled by them, we would become unable to solve all our problems.


And it would be AT  THAT  POINT  that we would lapse back into the state our predecessors of those many millions or billions of years ago were in, when they were at the mercy of having to depend upon "nature" to control our population.


( :? > ) 






















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