"Worn down by nearly three decades of peril"
Saw this today from The Onion, it's an oldie but a goodie:
Archaeologist Tired Of Unearthing Unspeakable Ancient Evils
...
Over the course of his career, Whitson has been frequently lauded by colleagues for his thorough, methodical examinations of ancient peoples. He has also been chased by the snake-bodied ophidian women of Al'lat in Israel, hunted down by Mayan coyote specters manifested out of lost time and shadow in the Yucatan, and hounded by the Arctic-sky-filling Walrus Bone Woman of the early Inuits.
"It's true, I've got to stop reading the inscriptions on ancient door seals out loud," Whitson said. "I also need to quit dusting off medallions set into strange sarcophagi, allowing the light to hit them for the first time in centuries. And replacing the jewels that have fallen from the foreheads of ancient frog-deity statues-that's just bad archaeological practice."
(via Savage Minds)
Dingo difficulties
From the discussion of L. C. Birch's paper, "Evolutionary opportunity for insects and mammals in Australia", in the edited volume The Genetics of Colonizing Species, edited by H. G. Baker and G. L. Stebbins, p. 212:
Waddington: At what date was the ordinary dog introduced into Australia? Dingoes were there before white men?
Birch: Dingoes probably came to Australia with the aborigines some millenia [sic] ago. The domesticated dog of the white man has been in Australia less than 2 centuries.
Mayr: Well, the dingo is a dog. If you go to the mountains of New Guinea you will see dogs which cannot be distinguished from dingoes. They do not bark. These dingo-like dogs are associated with the native villages and I would say that the dog or dingo came to Australia with one of the early waves of aborigines, whether this was 6000 or 12,000 B.C. or earlier.
Waddington: It is not a feral European dog?
Birch: It would be awfully hard to study this.
Mayr: You would need to wear chain mail.
Minireview
I found that exchange very entertaining, but if I'm posting it I figured I'd better provide some pointers to recent work on dingo evolution. Tim Flannery (2003) attributed the arrival of the dingo in Australia to contacts with Lapita people between 4000 and 3500 years ago. It has been suggested that ancient Polynesian dogs were also of this type, represented archaeologically by the "Pukapuka dog" (Shigehara et al. 1993). Flannery also mentions the work of Gordon Corbett, who proposed that Australian lice had been transferred back to Asia on one or more dingoes at some point. This transfer occurred in ancient times, and requires that some people landed on Australia, picked up some dingoes, and schlepped them back to Indonesia.
Peter Savolainen and colleagues (2004) studied the mitochondrial DNA variation in dingoes and compared their sequences to dogs from populations throughout the world. They find that dingoes have a very circumscribed degree of mtDNA variation, with one major haplotype (A29) and several minor haplotypes that are one- or two- mutation variants of this one. The haplotype A29 is otherwise found only in Asian, Polynesian and Arctic dogs. Their conclusion has this:
Among domestic dogs, A29 was found only among East Asian, Island Southeast Asian, and American dogs, and the mtDNA types radiating from A29 in the minimum-spanning network were found almost exclusively in East Asia (11), strongly indicating an East Asian rather than Indian origin for the dingo ancestor. The estimated time for the founding of the dingo population, 5,000 yr ago, fits relatively well with the archaeological record of the region, with the oldest finds of dingo being 3,500 years old and the earliest finds of dogs on nearby islands being 3,500-year-old remains on Timor (7). An East Asian ancestry 5,000 yr ago suggests that the dingoes may have arrived in connection with the expansion from south China into Island Southeast Asia of the Austronesian culture, which involved domestic dogs, pigs, and chicken. According to the current theories, the expansion started 6,000 yr ago from Taiwan via the Philippines to Indonesia, where it was split into a westward and an eastward direction and had by 4,000 yr ago reached Timor (7, 21).
In conclusion, this study of mtDNA sequence variation among dingoes provides a number of clues from which a detailed picture of the origin and history of the Australian dingo can be derived. The dingo originated from a population of East Asian dogs. Type A29 was one of several domestic dog mtDNA types brought into Island Southeast Asia, but only A29 reached Australia. The dingo population was probably founded from a small number of animals, as the last trickle of domestic dogs through a series of bottlenecks, or even by a single chance event and has since remained effectively isolated from other dog populations. The dingoes may have arrived in connection with the expansion, starting 6,000 yr ago, from south China into Island Southeast Asia of the Austronesian culture. By this time, domestic dogs had existed for several thousand years (4, 11), and the present semidomestic state of the dingo can probably be attributed to a long existence as a feral animal. After >3,500 years of isolation, the dingoes represent a unique isolate of early undifferentiated dogs.
They also note that the A29 haplotype is found in the New Guinea "singing" dogs -- the feral dogs that Mayr mentions. The New Guinea dogs were reviewed by Janice Koler-Matznick and colleagues (2003). They can be distinguished from dingoes, both in terms of their behaviors and in their size -- the New Guinea dogs average smaller than the smallest dingoes. The two are apparently related to each other, and Balinese street dogs also include the dingo-like mtDNA sequence, although their variation is much higher than found in dingoes (Irion et al. 2005). Other "pariah" dogs with similar phenotypes (e.g., light tan coloration) exist in India, Phillipines, and Southeast Asia, but these may have evolved convergently with the dingo.
That's my quick dingo mini-review. I don't claim it's complete, but it gives some directions for further looking for those interested.
References:
Birch LC. 1965. Evolutionary opportunity for insects and mammals in Australia. Pp. 197-214 in The Genetics of Colonizing Species, edited by Baker HG, Stebbins GL. Academic Press, New York.
Flannery TF. 2003. The Future Eaters: An Ecological History of the Australian Lands and People. Grove Press, New York.
Irion DN, Schaffer AL, Grant S, Wilton AN, Pedersen NC. 2005. Genetic variation analysis of the Bali street dog using microsatellites. BMC Genet 6:6. doi:10.1186/1471-2156-6-6
Koler-Matznick J, Brisbin IL, Jr, Geinstein M, Bulmer S. 2003. An updated description of the New Guinea singing dog (Canis hallstromi, Troughton 1957). J Zool Lond 261:109-118. doi:10.1017/S0952836903004060
Savolainen P, Leitner T, Wilton AN, Matisoo-Smith E, Lundeberg J. 2004. A detailed picture of the origin of the Australian dingo, obtained from the study of mitochondrial DNA. Proc Nat Acad Sci USA 101:12387-12390. doi:10.1073/pnas.0401814101
Shigehara N, Matsu'Ura S, Nakamura T, Kondo M. 1993. First discovery of the ancient dingo-type dog in Polynesia (Pukapuka, Cook Islands). Int J Osteoarcheol 3:315-320. doi:10.1002/oa.1390030410
Taking on new functions, protein-wise
I have to note this commentary by Fyodor Kondrashov that I ran across. The commentary discusses this 2004 paper by Amir Aharoni and colleagues:
The 'evolvability' of promiscuous protein functions
How proteins with new functions (e.g., drug or antibiotic resistance or degradation of man-made chemicals) evolve in a matter of months or years is still unclear. This ability is dependent on the induction of new phenotypic traits by a small number of mutations (plasticity). But mutations often have deleterious effects on functions that are essential for survival. How are these seemingly conflicting demands met at the single-protein level? Results from directed laboratory evolution experiments indicate that the evolution of a new function is driven by mutations that have little effect on the native function but large effects on the promiscuous functions that serve as starting point. Thus, an evolving protein can initially acquire increased fitness for a new function without losing its original function. Gene duplication and the divergence of a completely new protein may then follow.
This can be understood through a broader consideration of protein structure and function. Enzymes catalyze reactions in large part due to their structures, which include binding domains for different biomolecules. These binding domains evolve specificity for particular target molecules, so that they have a lock-and-key configuration. But the system is not a perfect one-key-fits-one-lock arrangement. Instead, an enzyme may catalyze additional reactions inefficiently, over and above the one it has been adapted to catalyze well. Small changes in the amino acid sequence can sometimes add significantly to the efficiency in catalyzing these other reactions, without detracting from the primary adaptation.
Aharoni et al. (2004) demonstrated that this kind of change readily occurs for some proteins. In such cases, it is fair to say that there is no adaptive valley of reduced fitness between one enzymatic form (ancestral) that catalyzes one reaction efficiently, and another form (derived) that catalyzes two reactions efficiently. For the current discussion, I'm going to call such a protein overloaded -- it is doing twice the jobs we might expect it to do.
The paper raises a natural question from this observation: If it is often this easy for proteins to evolve additional functions, then why don't we see more multifunction proteins? Why aren't more proteins overloaded?
I think that the answer from a fitness perspective is not so simple. We see many gene duplications that have subsequently diverged in function. If a single gene could take on two functions with no fitness cost, we shouldn't probably see so many instances where the functional differentiation has followed gene duplication. Clearly there is a fitness cost; otherwise there would be no advantage to having duplicate genes instead of a single gene. It is even possible to imagine that overloading a protein with different functions might make subsequent duplication more likely. Overloading might be a temporary solution that provides a transition between a low-fitness one-function protein and a two high-fitness proteins with different functions.
Kondrashov (2005) (and this is weird; Nature Genetics has given them different dates even though they're in the same issue. It's because of their online publication dates. Get it together, Nature!) discusses what we know about the distribution of multi-function proteins:
There are many examples of proteins that have multiple functions: crystallins, antifreeze proteins, the p53 tumor-suppressor protein and a broad class of enzymes that recognize different substrates all come to mind. On the other hand, many other proteins can be described with the broad generalization of one geneâone function. Why do proteins not take advantage of the opportunity to carry out multiple functions more often? It is true that evolution cannot produce the optimal solution, especially if doing so requires radical changes; think of a bilaterally symmetrical flatfish larva struggling to mold itself into an adult. But the results of Aharoni et al. show that the lack of stepping stones is probably not an obstacle for the evolution of new enzymatic functions, because even a small number of simple amino-acid substitutions are enough to improve promiscuous functions.
It is possible that broadening the range of functions of a molecule may be unnecessary, so that natural selection maintains the native function but never acts to improve the promiscuous one. This is analogous to mutational explanations of aging, which argue that aging occurs because natural selection does not act against mutations that impair performance only after reproductive age. This hypothesis, however, cannot explain why the evolution of new functions, when they are actually needed, does not generally proceed through the acquisition of multiple functions by a single enzyme.
He posits that multiple enzymes with distinct functions must in general be favored at the cellular level. He suggests that the evolution of multiple functions for single proteins may spur duplications as a way to maintain one-protein one-function systems. If he's right in this suggestion, which seems like the most likely alternative to me, then most gene duplications that become fixed probably are not neutral. Particularly if the different functions occur in different cell types; in which case simple regulatory differences between duplicate genes might provide functional differentation more-or-less automatically.
References:
Kondrashov FA. 2005. In search of the limits of evolution. Nat Genet 37:9-10. doi:10.1038/ng0105-9
Aharoni A, Gaidukov L, Khersonsky O, Gould SM, Roodvelt C, Tawfik DS. 2004. The 'evolvability' of promiscuous protein functions. Nat Genet 37:73-76. doi:10.1038/ng1482
John Hawks Department of Anthropology
University of Wisconsin—Madison
Copyright © 2007 John Hawks