4 research outputs found
Is The Amphibian Tree of Life really fatally flawed?
Wiens (2007 , Q. Rev. Biol. 82, 55â56) recently published a severe critique of Frost et al.'s (2006, Bull. Am. Mus. Nat. Hist. 297, 1â370) monographic study of amphibian systematics, concluding that it is âa disasterâ and recommending that readers âsimply ignore this studyâ. Beyond the hyperbole, Wiens raised four general objections that he regarded as âfatal flawsâ: (1) the sampling design was insufficient for the generic changes made and taxonomic changes were made without including all type species; (2) the nuclear gene most commonly used in amphibian phylogenetics, RAG-1, was not included, nor were the morphological characters that had justified the older taxonomy; (3) the analytical method employed is questionable because equally weighted parsimony âassumes that all characters are evolving at equal ratesâ; and (4) the results were at times âclearly erroneousâ, as evidenced by the inferred non-monophyly of marsupial frogs. In this paper we respond to these criticisms. In brief: (1) the study of Frost et al. did not exist in a vacuum and we discussed our evidence and evidence previously obtained by others that documented the non-monophyletic taxa that we corrected. Beyond that, we agree that all type species should ideally be included, but inclusion of all potentially relevant type species is not feasible in a study of the magnitude of Frost et al. and we contend that this should not prevent progress in the formulation of phylogenetic hypotheses or their application outside of systematics. (2) Rhodopsin, a gene included by Frost et al. is the nuclear gene that is most commonly used in amphibian systematics, not RAG-1. Regardless, ignoring a study because of the absence of a single locus strikes us as unsound practice. With respect to previously hypothesized morphological synapomorphies, Frost et al. provided a lengthy review of the published evidence for all groups, and this was used to inform taxonomic decisions. We noted that confirming and reconciling all morphological transformation series published among previous studies needed to be done, and we included evidence from the only published data set at that time to explicitly code morphological characters (including a number of traditionally applied synapomorphies from adult morphology) across the bulk of the diversity of amphibians (Haas, 2003, Cladistics 19, 23â90). Moreover, the phylogenetic results of the Frost et al. study were largely consistent with previous morphological and molecular studies and where they differed, this was discussed with reference to the weight of evidence. (3) The claim that equally weighted parsimony assumes that all characters are evolving at equal rates has been shown to be false in both analytical and simulation studies. (4) The claimed âstrong supportâ for marsupial frog monophyly is questionable. Several studies have also found marsupial frogs to be non-monophyletic. Wiens et al. (2005, Syst. Biol. 54, 719â748) recovered marsupial frogs as monophyletic, but that result was strongly supported only by Bayesian clade confidence values (which are known to overestimate support) and bootstrap support in his parsimony analysis was <â50%. Further, in a more recent parsimony analysis of an expanded data set that included RAG-1 and the three traditional morphological synapomorphies of marsupial frogs, Wiens et al. (2006, Am. Nat. 168, 579â596) also found them to be non-monophyletic. Although we attempted to apply the rule of monophyly to the naming of taxonomic groups, our phylogenetic results are largely consistent with conventional views even if not with the taxonomy current at the time of our writing. Most of our taxonomic changes addressed examples of non-monophyly that had previously been known or suspected (e.g., the non-monophyly of traditional Hyperoliidae, Microhylidae, Hemiphractinae, Leptodactylidae, Phrynobatrachus , Ranidae, Rana , Bufo ; and the placement of Brachycephalus within â Eleutherodactylus â, and Lineatriton within â Pseudoeurycea â), and it is troubling that Wiens and others, as evidenced by recent publications, continue to perpetuate recognition of non-monophyletic taxonomic groups that so profoundly misrepresent what is known about amphibian phylogeny. © The Willi Hennig Society 2007.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74688/1/j.1096-0031.2007.00181.x.pd
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Mechanisms â©ofâ© change â©in â©protein â©architecture
Proteins are the basic building blocks and functional units in all living organisms.
Moreover, differences between species can frequently be explained with
differences in their protein complements. Importantly, proteins are often
composed of segments, i.e. domains that have a certain level of evolutionary,
structural and/or functional independence. The majority of proteins in nature
contain two or more domains, and an individual domain can often occur in
combinations with different domain partners.
In the first part of my thesis, I traced the history of animal gene families
and the proteins these genes encode. By this means, I was able to infer events
where changes in protein domain architectures took place. This showed that
both insertions and deletions of single copy domains preferentially occur at
protein termini, but also that changes are more likely to occur after gene
duplication than organism speciation. Finally, domains that were most
frequently gained were the ones that are related to an increase in organismal
complexity, thus underlining the important role of domain shuffling in animal
evolution.
In the second part of my thesis, I focused on a set of high confidence
domain gain events and investigated the evidence for molecular mechanisms
that caused these domain gains. In agreement with observations from the first
part - that changes preferentially occur at the termini - I have found that the
strongest contribution to gains of novel domains in proteins comes from gene
fusion through the joining of exons from adjacent genes into a novel gene unit.
Two other mechanisms that have been suggested to play a major role in the
evolution of animal proteins, retroposition and middle insertions through
intronic recombination, have a smaller role in comparison to gene fusions. Since
the majority of these domain gains are again observed after gene duplication,
this suggests a powerful mechanism for neofunctionalization after gene
duplication.
iii
Finally, in the last part of my thesis, I address a mechanism that increases
the number and variety of proteins in an organism â alternative splicing. In
particular, I investigate the functional consequences of tissue-specific alternative
splicing events. I found that tissue-specific splicing tends to affect exons that
encode protein regions without defined secondary or tertiary structure.
Importantly, it is known that these disordered regions frequently play a role in
protein interactions. In agreement with this, I observed significant enrichment of
tissue-specifically encoded protein segments in disordered binding peptides and
posttranslationally modified sites. A possible result of the finely regulated
alternative splicing of these segments is a tissue-specific rewiring of protein
network. In conclusion, both alternative splicing and domain shuffling can
increase proteome diversity. However, a protein with a new function can often
directly or indirectly shape the functions of other proteins in its environment
A strategy for sequence phylogeny research.
Minimal mutation trees, and almost minimal trees, are constructed from two data sets, one of phenylalanine tRNA sequences, and the other of 5S RNA sequences, from a diverse range of organisms. The two sets of results are mutually consistent. Trees representing previous evolutionary hypotheses are compared using a total weighted mutational distance criterion. The importance of sequence data from relatively little-studed phylogenetic lines is stressed. A procedure is illustrated which circumvents the computational difficulty of evaluating the astronomically large number of possible trees, without resorting to suboptimal methods