The first paper by Per Christiansen, who has done excellent work on various extinct species correlating skeletal structure and biomechanics, appears open-access in PLoS ONE.¹ This paper was also covered by Greg Laden a few weeks ago. Christiansen’s study concentrates specifically on felids, and compares the saber-toothed cats to modern cats. Christiansen found that the saber-toothed skulls varied the most in shape along a dorso-ventral axis, with saber-toothed cats developing taller, shorter skulls.

Relative warp 2 is primarily related to dorsoventral skull shape, and specimens with lower warp scores have a dorsoventrally much taller and anteroposteriorly more compact skull, ventrally deflected glenoid fossa, greatly curved and anteroventrally compressed and dorsoventrally tall zygomatic arch, elevated facial portion of the skull, and abbreviated mid-section of the skull. They also have enlarged external nares and distinct posterior retraction of the infraorbital foramen, posteroventral deflection of the ventral orbital rim, and slightly smaller and dorsally deflected occipital condyles.

Modern cats varied along a different axis, with larger cats tending to possess skulls with longer muzzles, thicker zygomatic arches, and taller eye sockets. However, cats do not classify neatly as either “large cat” or “small cat”, but range along a continuum.

The saber-toothed cats as well are not simply classified as morphologically distinct from modern cats, since many early saber-toothed cats fall within the range of modern cat skull shape. The later, more derived machairodonts developed longer canines (the dirk-toothed morphology), and with longer canines skull shape changed to allow a larger gape. This resulted additionally in a decrease in bite strength. As mentioned before, the development of saber-teeth is thought to have led to a different means of prey capture, with a stabbing killing bite driven by powerful neck muscles delivered to pinned prey. This simultaneously decreases the chance of snapping the saber-teeth and decreases the necessary bite force, compared to the suffocating bites of modern cats that can take many minutes to kill.

The second paper is a similar study, but examines several species of nimravids and barbourofelids in addition to modern cats and saber-toothed cats.² The authors, Slater and Valkenburgh, seem unconvinced of the argument for the movement of barbourofelids to their own family and include them with the nimravids. They compare the skull shapes of three groups: modern cats, modern cats and saber-toothed cats, and all felids plus nimravids and barbourofelids.

Like Christiansen, they note the changes in skull shape that result from increasing size in the modern cats, but also note that the puma (Puma concolor) has an unusual skull shape, more typical of that of the smaller cats than the large cats. The cheetahs (extant cheetah Acinonyx and the extinct American cheetah Miracinonyx) also have an unusual domed skull shape resulting from enlarged nasal passages to aid breathing. The authors note that the presence of this adaptation in the American cheetah, which is more closely related to the puma than the modern cheetah, lends support to the interpretation of the American cheetah as a fast-sprinting hunter.

Slater and Valkenburgh find a similar clustering of modern cats separately from derived saber-tooth cats, and find that nimravids and barbourofelids cluster with the saber-toothed cats, indicating convergent evolution of a similar skull shape with the evolution of longer canines. The barbourofelids examined were dirk-toothed and clustered with the derived saber-toothed cats, while most of the nimravids were scimitar-toothed and tended to cluster with the modern cats. This is a similar pattern to that observed by Christiansen, with the more derived, dirk-toothed species acquiring more drastic modifications in skull shape to accommodate the longer canines.

Per Christiansen has interpreted the clouded leopard Neofelis nebulosa in the past as a possible modern example of a cat in the early stages of saber-tooth cat divergence, since it possesses unusually long upper canines for its body size.³ However, Slater and Valkenburgh find that this species falls on the continuum midway between small cats and large cats in skull shape, and that the pantherines all possess a more saber-tooth-like skull shape. They suggest that the saber-tooth morphology requires a suite of characteristics, and unusually long canines are not sufficient, especially in the absence of lateral flattening of the canines. More research into the ecology of the clouded leopard will be required to determine if its canines demonstrate a new experiment in the saber-tooth morphology.

A final question asked by Slater and Valkenburgh is whether the traits present in saber-toothed carnivores develop as a mosaic, with different traits acquired at different times, or pleiotropically, with all traits emerging together. Slater and Valkenburgh take the extensive overlap in skull shape of conical-toothed and saber-toothed forms as evidence for mosaic evolution of the saber-toothed morphology. This suggests that the early evolution of scimitar-toothed forms did not initially require much change in hunting tactics, and thus must have evolved under a different selective pressure. The saber-teeth may have initially been used for threat displays in intraspecific competition, and then fallen under selection for a stabbing killing bite with longer canines and skull modifications to allow a wider gape.

The saber-tooth morphology is an unusual hypercarnivore body plan adapted for rapid kills, probably arising in an environment with relatively large prey animals and high competition from other predators. While this morphology has evolved independently in the felids, nimravids, barbourofelids, marsupials, and creodonts, little comparison of these groups to each other has been done. It appears that the saber-tooth morphology of the felids, nimravids, and barbourofelids evolved in a similar context, and comparison with the more distantly related groups to have evolved this morphology may find similarities in these as well.

1. Christiansen, P. “Evolution of Skull and Mandible Shape in Cats (Carnivora: Felidae),” PLoS ONE 2008, 3, e2807. DOI: 10.1371/journal.pone.0002807
2. Slater, G. J.; Valkenburgh, B. V. “Long in the tooth: evolution of sabertooth cat cranial shape,” Paleobiology 2008, 34, 403-419. DOI: 10.1666/07061.1
3. Christiansen, P. “Sabertooth characters in the clouded leopard (Neofelis nebulosa Griffiths 1821),” Journal of Morphology 2006, 267, 1186-1198. DOI: 10.1002/jmor.10468

Yesterday I checked up on some of the paleontology journals that have had new issues come out in the past couple months and was elated to find not zero, as usual, or even one or two, but three papers on saber-toothed predators! I will be writing a post about these, and rounding up links to discussions on other blogs.

This has also coincided with a dearth of really interesting papers, although I haven’t really had time to do much more than skim the abstracts. However, this week produced some interesting papers that I’ve set aside for possible later coverage here, unless something even cooler comes up!

Malaria is a disease caused by protozoan parasites in the genus Plasmodium. They are unusual in possessing an organelle called the apicoplast, a degenerated plastid captured from some point in the past from a plant cell, probably a dinoflagellate. This is interesting because plastids themselves probably originated from cyanobacteria that were captured by a eukaryote ancestral to the plants sometime in the Precambrian. The apicoplast could prove a useful drug target, since it is derived from plants, and selectively targeting its biosynthetic routes should interfere little with host cell processes.

Plasmodium parasites complete part of their lifecyle in a vertebrate host, but require an insect vector to complete the lifecycle. Asexual reproduction takes place in the vertebrate host, with an initial round of replication in the liver cells immediately following infection. Schizonts in the liver cells divide into multiple merozoites, which are released and infect red blood cells. Here the organism passes through a trophozoite stage, degrading the host erythrocyte’s hemoglobin to harvest valuable amino acids. The reactive heme core is trapped in polymeric hemozoin to prevent oxidative damage to the parasite. Once it has grown enough, the trophozoite matures to a schizont, divides multiple times to produce merozoite offspring, and the erythrocyte ruptures. The maturation of the parasites in red blood cells is often coordinated and periodic, and leads to the cyclical fevers of malaria when high loads of merozoites are repeatedly dumped into the bloodstream.

The asexual lifecycle is a good mechanism for building up large numbers of the parasites in the host, but in order to travel to a new host, the parasite needs to undergo sexual reproduction. At the trophozoite stage many parasites go on to the asexual lifecycle, but some differentiate to gametocytes, which are infective to the mosquito host when ingested (unlike the asexual stages). The sex of these gametocytes is determined by environmental cues, and the sex ratio can vary widely. If the gametocyte is female, it produces a single gamete, but the male gametocytes can produce up to eight gametes. If the usual 50/50 sex ratio that we are most familiar with is preserved, this would lead to a huge excess of male gametes! Instead, the sex ratio tends to be biased towards females.

Sex ratios are a popular topic in evolutionary biology, and are generally well understood. While Plasmodium and other apicomplexan parasites often behave as predicted by theory, there are many examples of unusual findings. For instance, Hamilton’s theory of local mate competition says that when multiple unrelated strains are present, there should be selection for a higher proportion of males. Each male can fertilize multiple females, so producing males preferentially should propagate that genotype most efficiently at the expense of the unrelated genotypes. However, when only one genotype is present, the genotype would be competing with itself and selection for a more balanced sex ratio should result. Using local mate competition theory we can calculate the ideal sex ratio for a population of malaria parasites.

In their new Nature paper, Reece, Drew, and Gardner point out several observations from Plasmodium and other apicomplexans that are contrary to theory:

1. In some related avian apicomplexan parasites, sex ratios do not correlate with genetic diversity of an infection, and the ratio of females is consistently less than expected.
2. Over the course of an infection sex ratio can vary dramatically, and local mate competition theory does not explain this.
3. The ability of Plasmodium to alter sex ratios in response to host anemia shows local mate competition theory does not completely explain sex ratio.
4. A clonal line’s sex ratio does not appear to influence success in transmitting to the insect host.

In light of these observations, they decided to directly test the influence of sex ratio upon breeding success, and the influence of different variables upon sex ratio. The first experiment was a rather nifty assay involving two genetically modified Plasmodium berghei strains. One was incapable of producing viable female gametes, the other incapable of producing viable male gametes. By combining the two strains in different proportions they could directly control the male to female sex ratio of the population. The ookinetes produced could then be counted to determine reproductive success. They discovered that sex ratio was indeed female-biased, as predicted by theory, but that the males did not maximize their potential reproductive fitness. While capable of producing eight gametes, most males only produced two gametes, perhaps due to host immune response. This helps to explain why the sex ratio is not as female-biased as would be expected.

The next experiments used several clonal lines of Plasmodium chabaudi in mice. Six clonal lines were isolated and cultured, and the authors discovered that sex ratio varied over the course of infection for all. Three followed a similar pattern, but the other three showed their own unique time-course of sex ratios. This demonstrates genetic influence upon sex ratio in different strains, possibly adaptive variation. They discovered also that sex ratio is related to the level of anemia in the host. This is consistent with previous observations and with predictions. A female-biased sex ratio in combination with anemia in the host could lead to too few males being ingested by the insect vector to fertilize all of the females ingested. Thus, selection should favor tilting the sex ratio towards more males in the presence of host anemia. This was consistently shown to be true.

The high point of the paper is probably the studies of coinfection of mice with multiple Plasmodium strains. This is where local mate competition theory was directly tested. When strains were studied individually in a host, the sex ratio should be heavily female-skewed. However, when multiple strains are present, local mate competition theory predicts that more males will be produced. Exactly this pattern was observed, with a single-genotype infection sex ratio of about 15% males compared to a six-genotype infection sex ratio of about 44% males just before parasite load peak. Reece and coworkers also did a similar study with only two competing strains. With two out of three combinations a significant difference in sex ratio was observed, but it is not clear why the third strain did not modify sex ratio in response to co-infection. This strain was the least virulent, so there may be factors related to virulence and reproductive strategies that remain to be examined.

The pattern of sex ratios in apicomplexan parasites has been often confounding, and this paper helps to illuminate some of the reasons for apparent contradictions. While following the same general trends, sex ratio in different clonal lines is subject to genetic variation. Environmental factors such as anemia and host immune response can also influence sex ratio. When these factors are taken into account, the response of Plasmodium parasites to clonal and mixed infection is consistent with local mate competition theory. It is still unknown how the parasites determine their level of relatedness to other malaria parasites in the bloodstream, and this is an intriguing direction for future research.

I checked in on Nature earlier, since a new issue comes out tomorrow, and find that there’s an article combining two favorite topics of mine—malaria and sex ratios. I can only read the abstract from home, so I hope the suspense doesn’t keep me up too late. I anticipate that paper will show up on my blog shortly.

There is some debate about whether Lissamphibia, the group containing all extant amphibians, is monophyletic or not. The temnospondyls and lepospondyls are two major amphibian groups that diverged about 328-335 million years ago. Some paleontologists consider lissamphibians to have evolved from temnospondyls, while others take the opposite tack and consider them as having evolved from lepospondyls. Still others think that there is a split in Lissamphibia, with some members of the group descended from temnospondyls while others descended from lepospondyls.

This is the picture that Anderson and coworkers present. They suggest that the caecilians, a group of unusual legless amphibians with a tendency towards fossoriality, originated within the lepospondyls, while the other lissamphibians (including Gerobatrachus) evolved from temospondyls. Their phylogenetic tree is shown here (Reprinted by permission from Macmillan Publishers Ltd: Nature 453, 515-518, copyright 2008).

They place Batrachia (frogs + salamanders) in Temnospondyli as a sister group to Gerobatrachus. The caecilians, represented by Eocaecilia, appear in Lepospondyli. While this tree is the most parsimonious of the trees constructed (trees for Lissamphibia monophyletic in Temnospondyli and Lepospondyli were also constructed) the bootstrap values are lower than desirable.

The relationships of the amphibians are controversial and will probably remain so for some time. If it is ultimately determined that this phylogenetic tree is correct, there is the question of how to keep Lissamphibia monophyletic. Traditionally Lissamphibia has been limited to extant amphibians, and expanding Lissamphibia to include caecilians would bring in many extinct temnospondyls and lepospondyls. The situation might be more easily dealt with by expelling caecilians from Lissamphibia, or moving entirely away from Lissamphibia as a clade. Perhaps “lissamphibian”, like “reptile”, will remain as a holdover of Linnaean taxonomy.

Many human diseases can be linked to a specific gene, and most of these genes have a mouse ortholog. Some of these mouse genes have been experimentally knocked out, and the null mutants studied for any effects of the absence of that gene. Liao and Zhang examined a set of 120 genes determined to be essential in humans—when the gene is rendered useless due to a null mutation fitness is zeroed out due to death before sexual maturity or sterility. The authors examined the records for mouse knock-outs for these genes, this time looking for genes that are not essential in mice in spite of their orthologs being necessary in humans. They found that 27 of these genes are not essential in mice. In these cases knock-out mice survived to maturity and were able to reproduce normally, at least until the age of 6 months. Additionally, in a few cases the knock-out mice showed no detrimental effects of the null mutation at all.

An examination of the human ortholog of these genes shows that many (44.4%) of the human essential/mouse nonessential genes localize to the cell vacuole. This organelle is involved in waste processing. Mice have a very rapid metabolic rate compared to humans, meaning that we might expect their vacuoles to have more stringent efficiency requirements. On the other hand, humans reproduce at a much later age than mice, meaning that the vacuole has to process more wastes before successful reproduction.

The authors additionally examined the nonsynonymous distance and the synonymous distance between the orthologs. This is a measurement of the frequency of nonsynonymous (affecting protein product sequence) or synonymous (redundant mutations not affecting protein product sequence) mutations. We would expect essential genes to have a low nonsynonymous distance because of purifying selection restricting divergence. Nonessential orthologs should be more free to mutate without causing detrimental effects. Indeed, the nonsynonymous distance between orthologs essential in both species (HeMe) was low. The nonsynonymous distance between genes essential in humans and their nonessential mouse orthologs (HeMn) was higher. Indeed, this was even higher than the average nonsynonymous distance between any human gene and its nonessential ortholog (HaMn).

The authors propose two factors affecting gene sequence divergence. First, the greater nonsynonymous distance between human essential genes and their nonessential mouse orthologs could be due to a slackening of purifying selection in the mouse orthologs. Alternatively, it could be due to positive selection for mutations in the genes essential in humans. The comparison of the HeMn set to HaMn reveals that this is the case. The HaMn set is composed of HeMn genes and HnMn genes. The genes nonessential in both humans and mice should be relatively free of purifying selection, so if the mere absence of purifying selection is the explanation for the nonsynonymous distance, the nonsynonymous distance for HeMn should be about equal to the nonsynonymous distance for HaMn. Since its nonsynonymous distance is actually greater, that must mean that natural selection was favoring certain nonsynonymous substitutions in human orthologs during evolution.

Indeed, a study of branch-specific nonsynonymous distance/synonymous distance ratios shows accelerated nonsynonymous substitution in primate evolution. For genes involved in vacuole function, this evolutionary route combined a general increase in body size with later sexual maturity. This would change functional restraints upon the vacuole, and favor certain beneficial mutations. Other genes essential in humans and nonessential in mice do not have as obvious a functional divergence, but probably experienced similar changes in function.

The gene orthologs that are essential in humans and not essential in mice are easily visible to us because of the dire diseases that result from mutation of these genes in humans. We can then explore the effects of knocking out these genes in mice. Obviously we cannot do the opposite. Currently we do not have the technology to selectively knock out specific genes in humans, and even if we could, knocking out genes in human embryos and then following the individuals to adulthood to determine their longevity and reproductive success would be unconscionable. Though we cannot study these mouse essential/human nonessential genes, they no doubt exist. Evolution is not targeted towards production of the human species, and other species have their own evolutionary specializations.

Gene orthologs carry out similar functions in most cases, and often the gene product from one species can substitute directly for its ortholog in a different species (as I mentioned in my discussion of genes in volvocine algae and their unicellular relatives). However, developmental and functional constraints will differ in different organisms, and a gene variant that is lethal in one species may be viable in another. Liao and Zhang point out that while knowledge of orthologs in other species can be illuminating, it should serve as a first approximation of gene function. Studies in mice will continue to provide us with important information with less expense and fewer ethical worries than other animal studies. However, in some cases we may need to ultimately move to primate disease models. This is probably most important for disorders of vacuole function, which appears to differ significantly between mice and humans.

However, today I want to talk about the platypus’ sex chromosomes. Platypuses, like the therians, have genetic sex determination. They have an XX/XY system in which males (XY) are the heterogametic sex. Many reptiles have environmental sex determination, with sex determined by factors such as incubation temperature during embryonic development. However, some reptiles and all birds have a ZW/ZZ sex determination system, with females (ZW) as the heterogametic sex.

Something as basic as sex determination seems necessarily static and unchanging, but in actuality sex chromosomes and sex determination systems evolve, sometimes very rapidly. I mentioned in a previous post the gradual tightening of Muller’s ratchet, which in the absence of translocation of new DNA from another chromosome will eventually destroy the Y chromosome (or the W chromosome in ZW heterogametic organisms). There too I mentioned the way that some mole voles have already lost the Y chromosome, with sex determination now based upon a gene on some autosomal chromosome, which will now be under selection for the accumulation of male-benefiting genes and may evolve into a new set of sex chromosomes. Karyotype studies of the platypus shows a different but equally strange phenomenon—ten sex chromosomes.¹ While this oddity was obvious early on, the new paper from Genome Research firmly establishes a different phenomenon, which was anticipated by some researchers. While monotremes and therians both have XY/XX systems, the monotreme X and Y chromosomes evolved independently, and the monotreme X chromosomes have significant sequence similarities to the avian Z chromosome.²

This is consistent with basal amniotes possessing early prototypes of the avian W and Z chromosomes. These were passed on to the sauropsid and synapsid lines. Among the sauropsids, some evolved other methods for sex determination while others retained the W and Z chromosomes, or in the case of the snakes evolved their own versions of the W and Z chromosomes. On the synapsid line it is hard to say what other sex determination systems may have evolved, since there are only a few closely-related extant lineages of synapsids. Veyrunes, Waters, and coworkers found that the presence of sex chromosomes with sequence similarity to avian Z chromosomes in monotremes shows that the line leading to mammals kept the amniote proto-ZW/ZZ system for quite a while. After the monotreme/therian divergence the monotremes began evolving from a ZW/ZZ system to a XY/XX system. Since there are only two extant monotremes, the platypus and the echidna, it is hard to say when the monotreme’s multiple sex chromosomes evolved. The platypus has ten sex chromosomes, while the echnidna has nine (five X’s and four Y’s).³ The monotremes manage to keep these multiple chromosomes coordinated by homology between the ends of the chromosomes, so they line up in a chromosomal chain.

Along the line to marsupials and placental mammals our ancestors lost their dependence upon the ZW/ZZ system and evolved the therian X and Y chromosomes. Veyrunes and Waters report that genes on our X chromosome map to orthologs found on platypus chromosome 6, an autosomal chromosome. The ancestor of this chromosome 6 probably evolved into our X chromosome on the line to the modern therians. Since the marsupial and placental mammal sex chromosomes are homologous, the therian XY/XX system evolved by the time the marsupials and placental mammals diverged, although these chromosomes have undergone subsequent changes in both lineages. Meanwhile the ancestral W and Z sex chromosomes over time fragmented by translocations to other chromosomes and losses to deletions. The remnants of the ancestral Z chromosome are scattered over several autosomal chromosomes. Some of the details of these transformations can be seen in the phylogenetic tree from Genome Research shown to the right.²

Importantly, monotremes lack SRY (sex-determining Y), a gene critical in male gonadogenesis in therians. SRY evolved from the SOX3 gene, which likewise maps to platypus chromosome 6. I speculate that the trigger for the evolution of our XY/XX system is the evolution of SRY. As this gene began to take a role in male sexual differentiation selection would favor the limitation of recombination between the proto-Y chromosome and the proto-X chromosome and the segregation of male-specific genes on the new Y chromosome.⁴ However, it is also possible that SRY took over from some other gene that kicked off the differentiation of this previously autosomal chromosome pair into two new sex chromosomes.⁴

While the presentation of this discovery has not been as misleading as the Nature article on the full genome, there are some problems that T. Ryan Gregory points out at Genomicron. As I mentioned before, we should not expect a trait possessed by monotremes to be primitive simply based upon the monotremes’ divergence some 20 million years before the divergence of marsupials and placental mammals. When the monotremes diverged from the therians both lineages possessed an equal number of ancestral traits, and both lineages have evolved since then. Indeed, the information in this paper shows that the picture is more complicated than a simple summary of monotremes as “basal”. While the monotreme and therian lineages both inherited the ancestral W and Z chromosomes, both lineages then evolved their own X and Y chromosomes to replace these. The monotreme XY/XX system is as innovative as the therian XY/XX system.

1. Rens, W.; Grützner, F.; O’Brien, P. C. M.; Fairclough, H.; Graves, J. A. M.; Ferguson-Smith, M. A. “Resolution and evolution of the duck-billed platypus karyotype with an X₁Y₁X₂Y₂X₃Y₃X₄Y₄X₅Y₅ male sex chromosome constitution.” Proceedings of the National Academy of Sciences 2004, 101, 16257-16261. doi:10.1073/pnas.0405702101
2. Veyrunes, F.; Waters, P. D.; Miethke, P.; Rens, W.; McMillan, D.; Alsop, A. E.; Grützner, F.; Deakin, J. E.; Whittington, C. M.; Schatzkamer, K.; Kremitzki, C. L.; Graves, T.; Ferguson-Smith, M. A.; Warren, W.; Graves, J. A. M. “Bird-like sex chromosomes of platypus imply recent origin of mammal sex chromosomes.” Genome Research, published online before print May 7, 2008 doi:10.1101/gr.7101908
3. Rens, W.; O’Brien, P. C. M.; Grützner, F.; Clarke, O.; Graphodatskaya, D.; Tsend-Ayush, E.; Trifonov, V. A.; Skelton, H.; Wallis, M. C.; Johnston, S.; Veyrunes, F.; Graves, J. A. M.; Ferguson-Smith, M. A. “The multiple sex chromosomes of platypus and echidna are not completely identical and several share homology with the avian Z.” Genome Biology 2007, 8, R243. doi:10.1186/gb-2007-8-11-r243
4. Waters, P. D.; Wallis, M. C.; Graves, J. A. M. “Mammalian sex—Origin and evolution of the Y chromosome and SRY.” Seminars in Cell & Developmental Biology 2007, 18, 389-400. doi:10.1016/j.semcdb.2007.02.007

Does this seem odd to you?

I hope so! But this exact kind of thinking has led to some very muddled ideas related to the sequencing of the platypus genome, reported this week in Nature. The train of thought goes something like this:

1. Jurassic mammals diverged into a lineage leading to the monotremes and a lineage leading to the therians (marsupials and placental mammals) about 166 million years ago.
2. Since marsupials and placental mammals diverged from each other about 145 million years ago, that means monotremes are older.
3. Since monotremes are older, they must be more primitive than marsupials and placental mammals.

The problem is that the therians are exactly as old as the monotremes since we share a common ancestor some 166 million years ago. We seem to recognize easily that the therians have evolved significantly since they first appeared, but have a bias towards thinking that monotremes did not do the same during this same time period. In actuality when the monotremes and therians diverged both groups had the same set of ancestral traits. In each lineage some ancestral traits were replaced with new, derived traits, while other ancestral traits were retained. We have a tendency to emphasize the derived traits of placental mammals while overlooking ancestral traits. Then when we come across a different set of ancestral traits in a mammal on a different evolutionary branch, we find the set of ancestral traits that they happened to retain surprising and “primitive”. Add in a mix of novel derived features and you get, well, journalists saying silly things.

The Associated Press says:

The platypus is classed as a mammal because it has fur and feeds its young with milk. But it also has bird and reptile features—it lays eggs, has a duck-like bill and webbed feet, it and lives mostly underwater. Males also have spurs on their heels that inject pain-causing venom to ward off mating rivals.

Scientists believe the platypus and humans shared an evolutionary path until about 165 million years ago when the platypus branched off. Unlike other evolving mammals, the platypus retained characteristics of snakes and lizards, Graves said.

Meanwhile, Science News gets it completely wrong.

Though it’s a true mammal with fur, milk and sweat, the waddling duck-billed platypus also retains reptilian features, like venom production and egg-laying. . . . Take the venom genes—common in reptiles, but not in mammals. Spurs on platypus males’ hind legs inject venom like snake fangs do—venom that evolved as snake venom did, from tweaks in extra copies of the same types of ordinary nontoxic genes, the genome analysis shows.

Platypus venom genes, the study shows, are similar to reptilian venom genes but aren’t exactly the same. The genes are like skinny, blond, spoiled party-girls who grew up on different continents. Although they look alike, the genes became toxic independently.

ScienceDaily adds to the confusion, although partly redeeming themselves later in the article.

The duck-billed platypus: part bird, part reptile, part mammal—and the genome to prove it.

T. Ryan Gregory at Genomicron has written about misunderstandings of phylogenetic trees and the evolutionary process even among scientists, and thinks that these misunderstandings are responsible for some of the weird quotations showing up in the news. I think that it’s at the very least misleading when scientists are saying things like this:

The research showed the animal’s multifaceted features are reflected in its DNA with a mix of genes that crosses different classifications of animals, said Jenny Graves, an Australian National University genomics expert who co-wrote the paper.

“What we found was the genome, just like the animal, is an amazing amalgam of reptilian and mammal characteristics with quite a few unique platypus characteristics as well,” she told the Australian Broadcasting Corp.

So what’s wrong with saying that a monotreme has reptilian or avian traits? It makes zero sense evolutionarily. If we say marsupials have reptilian traits, then they must have descended from reptiles. As I have mentioned before, mammals are vehemently not descended from reptiles. Reptiles (and birds, who often get left out) and mammals share a common ancestor long ago that was neither a reptile nor a mammal, but an amniote. This amniote ancestor had many traits that got passed on to the sauropsid lineage and the synapsid lineage equally. Many of these traits were lost in the synapsid lineage, and others were acquired. Different traits were lost in the sauropsid lineage, and different other traits were acquired.

Platypuses do not have “reptilian” traits, they have ancestral amniote traits. The most obvious one is egg-laying. Platypuses retain a variety of amniote genes related to egg development that have been lost in the therians. In addition to retaining some ancestral amniote traits, platypuses have acquired new traits. One such trait is venom production—contrary to the Science News article above, platypus venom is not “reptilian” but an independently acquired trait and merely convergent upon reptile venom. Additionally, platypuses have an electrosensory system that allows them to detect prey based on electrical fields. Possessing these traits, a platypus might look at us and ask, “Who are you calling ‘primitive’?” since we preserve the ancestral (“primitive”) state by lacking both features.

I do not mean to diminish the significance of this paper. By studying the genomes of all extant synapsids and comparing these to extant sauropsids, we can learn more about our amniote common ancestor, and better understand when various traits evolved. But it is important to recognize that platypuses and echidnas are creatures with evolutionary histories as long as those of the therians. They do not represent basal monotremes, and have a variety of derived traits. Additionally, the amniote traits that are retained by monotremes do not make them “primitive” any more than the amniote traits retained by therians make that group “primitive”. As sister groups, the monotremes and therians both have ancestral amniote traits plus additional derived traits. We just overlook our “primitive” traits due to their familiarity.

I initially meant to address the information in the paper itself today, but this entry has become rather long. Now that I’ve gotten the ranting out of the way I will post on the paper itself in the next few days. I will try to get the bulk of that entry done today, but since I am going out of town this weekend I may be delayed.