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Biological Parsimony and Genomics

August 24, 2015

The previous post discussed the notion that biological processes, and biosystems in general, exhibit a profound economy of organization and structure, which can be termed biological parsimony. At the same time, there are biological phenomena which seem to run counter to this principle, at least at face value. In this post, this ‘counterpoint’ theme is continued, with an emphasis on the organization of genomes. In particular, the genome sizes of the most complex forms of life (unlike simpler bacteria) superficially considerably exceed the apparent basic need for functional coding sequences alone.

Complex Life With Sloppy Genomes?

When it comes to genomics, prokaryotes are good advertisements for parsimony. They have small and very compact genomes, with minimal intergenic spaces and few introns. Since their replication times are typically very short under optimal conditions, the time and energy requirements for genomic replication are often significant selective factors, tending to streamline genomic sizes as much as possible. A major factor for the evolution of prokaryotic organisms is their typically very large population size, which promotes the rapid positive selection of small fitness gains. Prokaryotic genomes are thus under intense selection for functional and replicative simplicity, leading to rapid elimination of non-essential genomic sequences.

Yet the situation is very different for more complex biologies of eukaryotes, where genome sizes are commonly bigger by 1000-fold or more than that of the bacterial laboratory workhorse, E. coli. It is widely recognized that this immense differential is enabled in eukaryotic cells through the energy dividend provided by mitochondria, the organelles acting as so-called powerhouses of such cells. Mitochondria (and chloroplasts in plants) are intracellular symbiotes, descendents of ancient bacterial forms which entered into an eventual partnership with progenitors of eukaryotic cells, and in the process underwent massive genomic reduction. The energetic contribution of mitochondria enabled much larger cells, with concomitant much larger genomes.

If eukaryotic genomes can be ‘sloppy’, and accommodate very large tracts of repetitive DNAs deriving from parasitic mobile elements, or other non-coding sequences, where is the ‘parsimony principle’ to be found? We will return to this question later in this post, but first let’s look at some interesting issues revolving around the general theme of genomic size.

Junk is Bunk?

While a significant amount of genomic sequence in a wide variety of complex organisms is now known to encode not proteins but functional RNAs, genome sizes still seem much larger than what should be strictly necessary. This observation is emphasized by the findings of genomic sequencing projects, where complex organisms, including Homo sapiens, show what seems at first glance to be a surprisingly low count of protein-coding genes. In addition, closely related organisms can have markedly different genome sizes. These observations are directly pertinent to the ‘C-value paradox’, which refers to the well-documented disconnect between genome size and organismal complexity. Since genomic size accordingly appears to be arbitrarily variable (at least up to a point), much non-coding DNA has been considered by many in the field to be ‘junk’. In this view, genomic expansion (by duplication events or extensive parasitism by mobile genetic elements) has little if any selective impedance until finally limited by truly massive genomic sizes. In other words, the junk DNA hypothesis holds that genomes can accumulate large amounts of superfluous sequence which are essentially along for the ride, being replicated in common with all essential genomic segments. This trend is only restricted when genomes reach a size which eventually does impact upon the relative fitness of an organism. Thus, even the junk DNA stance concedes that genomes must necessarily be size-restricted, even though a lot of genomic noise can be tolerated before this point is reached.

It must be noted that the junk DNA viewpoint has been challenged, broadly along two separate lines. One such counterpoint holds that the apparent lack of function of large sectors of eukaryotic genomes is simply incorrect, since a great deal of the ‘junk’ sequences are transcribed into RNAs with a variety of essential cellular functions beyond encoding proteins. As noted above, there is no question that functional (non-coding) RNAs are of prime importance in the operations of all cellular life. At a basic level this has been known almost since the birth of molecular biology, since ribosomal RNAs (rRNAs) and transfer RNAs (tRNAs) have been described for many decades. These RNAs are of course essential for protein synthesis, and are transcribed from corresponding genomic DNA sequences.

But in much more recent times, the extent of RNA function has become better appreciated, to include both relatively short regulatory molecules (such as microRNAs [miRNAs]) and much longer forms (various functional non-coding species [ncRNAs]). While the crucial importance of these classes of nucleic acid functionalities is beyond dispute, the relevance of this to genome sizes is another matter entirely. To use the human genome as a case in point, even if the number of functional RNA genes was twice the size of the protein-coding set, the net genome size would still be much larger than required. While the proponents of the functional-RNA refutation of junk DNA have pointed to the evident transcription of most (if not all) of complex vertebrate genomes, this assertion has been seriously challenged by the Hughes (Toronto) lab as based on inadequate evidence.

Other viewpoints suggest that the large fraction of eukaryotic chromosomal DNA which is seemingly superfluous is in fact necessary, but without a strong requirement for sequence specificity. We can briefly consider this area in a little more detail.

Genomic Junk and Some ‘Indifferent’  Viewpoints

One of these proposals, the ‘skeletal DNA’ hypothesis, as largely promulgated by Tim Cavalier-Smith, side-steps the problem of whether much of the genome is superfluous junk or not, in favor of a structural role for the large non-genic component of the genome. Here the sequence of the greater part of the ‘skeletal’ DNA segments is presumed to be non-specific, where the main evolutionary selective force is for genomic size per se, irrespective of the sequences of non-genic regions. Where DNA segments are under positive selection but not in a sequence-specific manner, the tracts involved have been termed ‘indifferent DNA’, which seems an apt tag in such circumstances. Cavalier-Smith proposes that genomic DNA acts as a scaffold for nuclei, and thus nuclear and cellular size correlate with genome sizes. But at the time, DNA content itself does not directly alter proliferating cell volumes; rather the latter results from variation in encoded cell cycle machinery and signals (related to cellular concentrations of control factors).

Another proposal for the role of large non-coding genomic segments could be called the ‘transposable element shield’ theory. In this concept (originally put forward by Claudiu Bandea) so-called junk genomic segments reduce the risk that vital coding sequences will be subjected to insertional inactivation by parasitic mobile elements. Once it has been drawn to one’s attention, this proposal has a certain intuitive appeal. Thus, if 100% of a complex genome was comprised of demonstrably functionally sequences, then by definition any insertion by a parasitic transposable sequence element would knock out a function (or at least have a very high probability of doing so). If only 10% of the genome was of vital functional significance, and the rest a kind of shielding filler, then the insertional risk goes down by an order of magnitude. This model assumes that insertion of mobile elements is sequence-target neutral, or purely random in insertion site. Since this is not so for certain types of transposable elements, the Bandea proposal also encompasses the notion that protective genomic sequences are not necessarily arbitrary, but include sequences with a decoy-like function, to absorb parasitic insertions with reduced functional costs. Strictly speaking, then, this proposal is not fully ‘indifferent’ in referring to ‘junk’ DNA, but clearly is at least partially so. It should be noted as well that shielding against genomic parasitism is of significance for multicellular organisms with large numbers of somatic cells, as well as germline protection.

In the context of whether genomes increase in size by the accumulation of ‘junk’ or through selectable (but sequence-independent) criteria, it should be noted that a strong case has been made Michael Lynch and colleagues for the significance of non-adaptive processes in causing changes in genome size, especially in organisms with relatively low replicative population sizes (the opposite effect to large-population prokaryotes, as noted above). The central issue boils down to energetic and other functional costs – if genome sizes can expand with negligible or low fitness cost, passive ‘junk’ can be tolerated. But a ‘strong’ interpretation of the skeletal DNA hypothesis holds that genome sizes are as large as they are for a selectable purpose – acting as a nuclear scaffold.

In considering the factors influencing the genome sizes of complex organisms, some specific cases in comparative genomics are useful to highlight, as follows.

Lessons from Birds, Bats, and Other ‘Natural Experiments’

Modern molecular biology has allowed the directed reduction of significant sections of certain bacterial genomes for both scientific and technological ends. But some ‘natural experiments’ have also revealed very interesting aspects of vertebrate genomes.

One such piece of highly significant information comes from studies of the genomes of vertebrates that are true fliers, as found with birds and bats. Such organisms are noted collectively for their significantly smaller genomes in comparison to other vertebrates, especially other amniotes (reptiles and mammals). The small-genome / flight correlation has even been proposed for long-extinct ancient pterosaurs, from studies of fossil bone cell sizes. In the case of birds, genome size reduction has been assigned as stemming from loss of repetitive sequences, deletions of certain genomic segments, and (non-essential) gene loss.

A plausible explanation for the observed correlation between the ability to fly and smaller genomes is the high-level metabolic demand of flight. This dictate is argued to favor streamlined genomes, via the reduction in replicative metabolic costs. Supporting evidence for such a contention is provided by the negative correlation between genome size and metabolic rate in all tetrapods (amphibians, reptiles, birds, and mammals), where a useful measure of oxidative metabolic rate is the ‘heart index’, or the ratio of heart mass to body weight. Even among birds themselves, it has been possible to show (using heart indices) negative correlations between metabolic rates and genomic sizes. Thus, highly active fliers with relatively large flight muscle quantities tend to have smaller genomes than more sedate fliers, with hummingbirds (powerhouses of high-energy hovering flight) having the smallest genomes of all birds.

It was stated earlier that closely related organisms can have quite different genome sizes, and the packaging of genomes in such cases can also differ markedly. The Indian muntjac deer has a fame of sorts among cytogeneticists, owing to the extremely low size of its chromosome count relative to other mammals (only 6 diploid chromosomes in females, with an extra one in males). Indeed, the Chinese muntjac has a more usual diploid chromosome count of 46, and yet this deer is closely enough related to Indian muntjacs that they can interbreed (albeit with sterile offspring, reminiscent of mules produced through horse-donkey crosses). The Indian muntjac genome is believed to be the result of chromosomal fusions, with concomitant deletion of significant amounts of repetitive DNAs, and reduction in certain intron sizes. As a result, the Indian muntjac genome is reduced in total size by about 22% relative to Chinese muntjacs.

This illustration from comparative genomics once again suggests that genome size alone cannot be directly related to function. Although the link between numbers of distinct functional elements and complexity might itself be inherently complex, it is reasonable to contemplate what degrees of molecular function are required to build different organisms. If all genomes were entirely functional and ‘needed’, then much more genomic sequence is required to build lungfishes, onions, and many other plants than human beings.

Junk vs. Garbage

A common and useful division of items that are nominally ‘useless’ has been noted by Sydney Brenner. He pointed out that most languages distinguish between stuff that is apparently useless yet harmless (‘junk’), and material that is both useless and problematic or offensive in some way (‘garbage’). An attic may accumulate large amounts of junk which sits there, perhaps for decades, without much notice, but useless items which become odoriferous or take up excessive space are promptly disposed of. The parallel he was making with genomic sequences is clear. ‘Garbage sequences’ that are, or become, deleterious in some way are rapidly removed by natural selection, but this does not apply to sequences which are merely ‘junk’.

Junk sequences thus do not immediately impinge upon fitness, at least in organisms with low population sizes. Also, ‘junk’ may be co-opted during evolution for a true functional purpose, as with the full ‘domestication’ of otherwise parasitic mobile elements. Two important points must be noted with respect to the domestication of formerly useless or even deleterious sequence elements: (1) just because some mobile element residues have become domesticated, it does not at all follow that all such sequences are likewise functional; and (2) the co-option (or ‘exaptation’) of formerly useless DNA segments does not in any way suggest that evolution has kept such sequences ‘on hand’ on the off-chance they might find a future use.

Countervailing Trends for Genomic Size

How do complex genomes expand in size, anyway? Duplication events are a frequent contributor towards such effects, and these processes can range from local effects on relatively small segments, to whole genes, and even entire genomes. The latter kind of duplication leads to a state known as polyploidy, which in some organisms can become a surprisingly stable arrangement.

Yet the major influence on genomic sizes in eukaryotes is probably the activity of parasitic mobile (transposable) elements, such that a correlation between genomic size and their percent constitution by such elements has been noted. It has been suggested that although in some cases very large genomes with a high level of transposable elements appear to be deleterious (notably certain plants believed to be on the edge of extinction), in other circumstances (large animal genomes as seen with salamanders and lungfish) a high load of transposable elements may be tolerated without significant fitness loss. The latter effect has been attributed to a slow acquisition of the mobile elements, whereby their continued spread tends to be inactivated by mutation or other (‘sequence decay’ mechanisms. This in itself can be viewed from the perspective of the ‘garbage/junk’ dichotomy: at least some transposable elements that remain active may be deleterious, and thus suitable for relegation into the ‘garbage’ box, while inactivated elements are more characteristic of ‘junk’.

Yet there is documented evidence indicating a global trend in evolution towards genome reduction, in a wide diversity of organisms. When this pattern is considered along with factors increasing genomic size, it has been proposed that the overall picture is biphasic. In this view, periods of genomic expansion in specific lineages are ‘punctuated’ not by stasis (as the original general concept of ‘punctuated equilibrium’ proposed) but with slow reduction in genomic sizes. Though the metabolic demands of flying vertebrates may place special selective pressures towards genomic reduction, a general trend towards genomic contraction suggests that selection always tends to favor smaller and more efficient genomes. Even where the selective advantage of genome size is small and subtle, over evolutionary time it will be inevitably exerted with the observed results. But at the same time, genomic copy-errors (from small segments to whole genes to entire genomes) and parasitic transposable elements act as an opposing influence towards genomic expansion. And in this context, it is important to recall the above notes (from Michael Lynch and colleagues) with respect to the importance of organismal population size in terms of the magnitudes of the selective pressures dictating the streamlining of genomes.

A human genome-reduction project (actually rendered much more feasible by the advent of new genome-editing techniques) could presumably produce a fully-functional human with a much smaller genome, but such a project would be unlikely to pass the scrutiny of institutional bioethics committees. (Arbitrary deletions engendered by blind natural selection will either be positively selected or not; a human project with the tools to reduce genome size would often lack 100% certainty that a proposed deletion would not have deleterious effects). Yet apart from this, we might also ask whether such engineered humans would have an increased risk of somatic cell mutagenesis via transposable elements (leading to cancer), if the Bandea theory of genomic shielding of transposable elements holds water.

Now, what then for parsimony in the light of the cascade of genomic information emerging in recent times?

Thrifty Interactomes?

If the junk DNA hypothesis was truly wrong in an absolute sense (that is, if all genomes were constituted from demonstrably functional sequences), then the parsimony principle might still hold at the genomic level. Here one might claim that all genomic sequences are parsimonious to the extent that they are functionally relevant, and therefore genomes are as large as functionally necessary, but no larger. Yet an abundance of evidence from comparative genomics (as discussed briefly above) suggests strongly that this intrepretation is untenable. But if a typical eukaryotic energy budget derived from mitochondria allows a ‘big sloppy genome’, where does the so-called parsimony principle come in?

The best answer to this comes not from genomic size per se, but gene number and the organization of both gene expression and gene expression products. Consider some of the best-studied vertebrate genomes, as in the Table below. If protein-coding genes only are considered, both zebrafish and mice have a higher count than humans. Nevertheless, as noted above, it is now known that non-coding RNA, both large and small, are very important. If these are noted, and a combined ‘gene tally’ thus calculated, we now find Homo sapiens coming out on top. More useful still may be the count for gene transcripts in general, since these include an important generator of genomic diversity: differential gene splicing.

ComparativeGeneCounts-TABLE

_________________________________________________________________________

But what does this mean in terms of complexity? Are humans roughly only twice as complex as mice, or roughly three times as complex as a zebrafish? Almost certainly there is much more to the picture than that, since these superficial observations belie what is likely to be the most significant factor of all: the way expressed products of genomes (both proteins and RNAs) interact, which can impose many hidden layers of complexity onto the initial expression toolkit. These patterns of interactions comprise an organism’s interactome.

How many genes does it take to build a human? Or a mouse, or a fish? As noted earlier in this post, in the aftermath of the first results for the sequencing of the human genome, and numerous other genomes soon afterward, many onlookers expressed great surprise at the ‘low’ number of proteins apparently encoded by complex organisms. Other observers pointed out in turn that if it is not known how to build a complex creature, how could one know what an ‘appropriate’ number of genes should be? Still, a few tens of thousands of genes does seem a modest number, even factoring in additional diversity-generating mechanisms such as differential splicing. At least, this would be the case if every gene product had only a single, unique role in the biology of an organism – but this is manifestly not so.

In fact, single proteins very often have multiple roles, in multiple ways, via the global interactome. An enzyme, for example, may have the same basic activity, but quite distinct roles in cells of distinct differentiation states. Other proteins can exhibit distinct functional roles (‘moonlighting’) in different circumstances. It is via the interactome, then, that genomes exhibit biological parsimony, to a high degree.

This ‘interactomic’ theme will be developed further in the succeeding post.

Some Parsimonious Conclusions

(1) Prokaryotic genomes have strong selective pressures towards small size.

(2) Eukaryotic genomes can expand to much larger sizes, with considerable portions of redundant or non-essential segments, by mechanisms that may be non-adaptive or positively selected (skeletal DNA, transposable element shielding). Such processes include duplication of specific segments (gene duplication) or even whole-genome duplication (polyploidy). This may countered by long-term evolutionary trends towards genome reduction, but the ‘expandability’ of eukaryotic genomes (as opposed to prokaryotes) still remains.

(3) The expressed interactomes of eukaryotes are highly parsimonious.

(4) Biological parsimony is a natural consequence of strong selective pressures, which tend to drive towards biosystem efficiency. But the selective pressures themselves are linked to the energetics of system processes, and population sizes. Thus, a biological process (case in point: genome replication) within organisms with relatively small populations and moderate energetic demands (many vertebrates) may escape strong selection for efficiency, and be subjected to genetic drift and genomic expansion, with a slow counter-trend towards size reduction. An otherwise tolerable process in terms of energetic demands (genome replication once again) may become increasingly subject to selective pressure towards efficiency (size contraction) if an organism’s metabolic demands are very high (as with flying vertebrates).

(5) Based on internal functions alone, it might be possible to synthetically engineer a complex multicellular eukaryote where most if not all of its genome had a defined function, but such an organism would likely be highly vulnerable outside the laboratory to disruption of vital sequences through insertion of parasitic mobile elements.

And to conclude, a biopolyversical rumination:

There are cases of genomes expanding

Into sizes large and outstanding

Yet interactomes still show

That parsimony will grow

Via selective pressures demanding

References & Details

(In order of citation, giving some key references where appropriate, but not an exhaustive coverage of the literature).

They have small and very compact genomes, with minimal intergenic spaces and few introns.’     In cases where conventional bacteria have introns, they are frequently ‘Group I’ introns in tRNA genes, which are removed from primary RNA transcripts by self-splicing mechanisms. The ‘third domain of life’, the Archaeal prokaryotes, have tRNA introns which are removed via protein catalysts. See Tocchini-Valentini et al. 2015.

‘….their replication times are typically very short under optimal conditions….’     E. coli can replicate in about 20 minutes in rich media, for example. But not all prokaryotes are this speedy, notably some important pathogens. Mycobacterial doubling times are on the order of 16-24 hr for M. tuberculosis (subject to conditions) or as slow as 14 days for the causative agent of leprosy, M. leprae. For an analysis of the genetics of fast or slow growth in mycobacteria, see Beste et al. 2009. For much detail on Mycobacterium leprae, see this site.

A major factor for the evolution of prokaryotic organisms is their typically very large population size……’     For excellent discussion of these issues, see work from the lab of Michael Lynch, as in Lynch & Conery 2003.

‘…..this immense differential is enabled in eukaryotic cells through the energy dividend provided by mitochondria……’    See Lane & Martin 2010; Lane 2011.

‘……Mitochondria …… entered into an eventual partnership with progenitors of eukaryotic cells, and in the process underwent massive genomic reduction….’     Human mitochondrial genomes encode only 13 proteins. For a general and very detailed discussion of such issues. See Nick Lane’s excellent book, Power, Sex, Suicide (Oxford University Press, 2005.

The energetic contribution of mitochondria enabled much larger cells, with concomitant much larger genomes.’     In the words of the famed bio-blogger PZ Myers, ‘a big sloppy genome’ [a post commenting on the hypothesis of Lane & Martin 2010]

‘….complex organisms, including Homo sapiens, show what seems at first glance to be a surprisingly low count of protein-coding genes.’      See (for example) the ENSEMBLE genomic database.

‘…..closely related organisms can have markedly different genome sizes.’     See Doolittle 2013.

‘….even if the number of functional RNA genes was twice the size of the protein-coding set, the net genome size would still be much larger than required.’      The study of Xu et al. 2006 provides (in Supplementary Tables) the striking contrast between the estimated % of coding sequences and genome sizes for a range of prokaryotes and eukaryotes. Although slightly dated in terms of current gene counts, the low ratios of coding sequences in most of the sampled eukaryotes (especially mammals( would stand if even doubled. By the same token, with prokaryotes, a direct correlation exists between coding DNA and genome size, but this relationship falls down for eukaryotes above a certain genome size (0.01 Gb, where the haploid human genome is about 3 Gb; see Metcalfe & Casane 2013).

‘….the proponents of the functional-RNA refutation of junk DNA have pointed to the evident transcription of most if not all of complex vertebrate genomes…..’     The ENCODE project ignited much controversy by asserting that the notion of junk DNA was no longer valid, based on transcriptional and other data. (See Djebali et al. 2012; ENCODE Project Consortium 2012).  The ‘junk as bunk’ proposal has itself been comprehensively debunked by Doolittle (2013) and Graur et al. 2013.

 ‘….. this assertion [widely encompassing genomic transcription] has been seriously challenged as based on inadequate evidence.’     See Van Bakel et al. 2010.

‘…..skeletal DNA hypothesis, as largely promulgated by Tim Cavalier-Smith….’     See Cavalier-Smith 2005.

‘…..this concept (originally put forward by Claudiu Bandea) …..’      See a relevant online Bandea publication.

‘…..shielding against genomic parasitism is of significance for multicellular organisms…..’      Regardless of the veracity of the Bandea hypothesis, a variety of genomic mechanisms for protection from parasitic transposable elements have evolved; see Bandea once more.

Where DNA segments are under positive selection but not in a sequence-specific manner, the tracts involved have been termed ‘indifferent DNA…..’      See Graur et al. 2013.

‘….a strong case has been made Michael Lynch and colleagues for non-adaptive changes in genome size….’      See Lynch 2007.

‘….molecular biology has allowed the directed reduction of significant sections of certain bacterial genomes ….’      For work on genome reduction in E. coli, see Kolisnychenko et al. 2002; Pósfai et al. 2006. For analogous work on a Pseudomonas species see Lieder et al. 2015. The Venter have (famously) worked on synthetic genomes, which allows the most direct way of establishing the minimal genome for a prokaryotic organism. With respect to this, see Gibson et al. 2010.

‘…birds and bats. Such organisms are noted collectively for their significantly smaller genomes in comparison to other vertebrates.‘     For avian genomes, see Zhang et al. 2014; for bats, see Smith & Gregory 2009. ‘…small-genome / flight correlation has even been proposed for long-extinct ancient pterosaurs’   See Organ & Shedlock, 2009. In this study it was found that ‘megabats’ (larger, typically fruit-eating bats lacking sonar) are even more constrained in terms of genomic size than microbats.

In the case of birds, genome size reduction has been assigned……’     For details in this area, see Zhang et al. 2014.

‘…..evidence of a negative correlation between genome size and metabolic rate …..A measure of oxidative metabolic rate is the ‘heart index…..’      See Vinogradov & Anatskaya 2006.

‘…highly active fliers with large relative flight muscle quantities tended to have smaller genomes than more sedate fliers. ‘      See Wright et al. 2014.

‘…hummingbirds (powerhouses of high-energy hovering flight) having the smallest genomes of all birds…’      See Gregory at al. 2009.

‘…..the Indian muntjac genome is reduced in total size by about 22% relative to Chinese muntjacs…..’      The Indian muntjac genome is about 2.17 Gb; the Chinese muntjac genome is about 2.78 Gb. See Zhou et al. 2006; Tsipouri et al. 2008.

‘……much more genomic sequence is required to build lungfishes, onions, and many plants than human beings.’     The note regarding onions comes from T. Ryan Gregory (cited as a personal communication by Graur et al. 2013). For lungfish and many other animal genome sizes, see a comprehensive database (overseen by T.R. Gregory). For plant genomes, see another useful database.

‘….A common and useful division of items that are nominally ‘useless’ has been noted by Sydney Brenner.‘      See Brenner 1998. This ‘junk / garbage’ distinction was alluded to by Graur et al. 2013.

‘…… ‘junk’ may be co-opted during evolution for a true functional purpose, as with the full ‘domestication’ of otherwise parasitic mobile elements……’     See Hua-Van et al. 2011.

‘…. because some mobile element residues have become domesticated, it does not at all follow that all such sequences are likewise functional.’      This point has been emphasized by Doolittle 2013.

‘…..a state known as polyploidy…….’      For an excellent review on many aspects of polyploidy, see Comai 2005.

‘……a correlation between genomic size and their percent constitution by such [mobile] elements has been noted.‘ See Metcalfe & Casane 2013.

‘…..has been suggested …….. very large genomes with a high level of transposable elements appear to be deleterious …… in other circumstances ……a high load of transposable elements may be tolerated….’      See Metcalfe & Casane 2013.

‘……documented evidence indicating a global trend in evolution towards genome reduction….’ | ‘…..it has been proposed that the overall picture is biphasic. Periods of genomic expansion in specific lineages are ‘punctuated’ not by stasis (as the original general concept of ‘punctuated equilibrium’ proposed) but with slow reduction in genomic sizes. ‘     See Wolf & Koonin 2013. For a background on the theory of punctuated equilibrium, see Gould & Eldredge 1993.

‘…..human genome-reduction project (actually rendered much more feasible by the advent of new genome-editing techniques)……’      There is so much to say about these developments (including zinc finger nucleases, TALENs, and in particular CRISPR-Cas technology) that it will form the subject of a future post.

‘ ENSEMBLE Dec 2013 release‘     (Table ) See the ENSEMBLE database site.

These patterns of interactions comprise an organism’s interactome.’      Note here that the term ‘interactome’ can be used in a global sense, or for a specific macromolecule. Thus, a study might refer to the ‘interactome of Protein X’, in reference to sum total of interactions concerning Protein X in a specific organism.

Next post: September.

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