Gibbons are sometimes referred to as “lesser apes” since they’re the smaller-bodied cousins of “great apes” like us humans, chimpanzees, gorillas, and orangutans. But what they lack in body mass they make up for in taxonomic diversity, with roughly 20 species distributed across four genus groups (Kim et al., 2011). And while male great apes (except humans) have large canine teeth, both sexes in gibbons have large maxillary canines — flashy weaponry for defending territory.
Pointy canine teeth peeking out from the upper and lower jaws of an adult female gibbon cared for at the International Primate Protection League (source)
My research has generally focused on brains and growth throughout human evolution, but I started looking at gibbons a few years ago when the COVID-19 pandemic put research travel on hold. Inspired by Julia Zichello’s 2018 article about gibbon models for understanding hominin evolution and appreciating that “overlooked small apes need more attention,” I had the opportunity to CT scan a unique skeletal collection of white-handed gibbons (Hylobates lar), which was sadly harvested from the forests of Thailand back in the late 1930s. Previous research on skull growth in gibbons has mostly used small samples compiled from different species (and sometimes even different genera). In contrast, this CT dataset includes many individuals at each stage of maturation from late infancy through adulthood, effectively representing a single population at a point in time. So with this larger cross-sectional sample of a single species, we can better understand how gibbon brains and faces grow. And because permanent teeth form in a long, continuous sequence throughout the growth period, an individual’s state of dental development can serve as a marker of where they are along the maturation process.
In a paper hot off the press, Julia Boughner and I analyzed dental development in this unique sample (article here). One of the coolest things we found was that gibbons’ large upper canine teeth are among the first to begin but last to finish tooth formation. In fact, the large canines growing inside relatively small faces may inhibit growth of one of the neighboring incisor teeth until the face has grown to create enough space for it. And while most teeth developing within the jaw begin emerging into the mouth once there’s enough room for them, gibbons’ gargantuan upper canines are forced out of hiding as they outgrow their bony crypts (check out the right-most jaw in the second row below).
Cross-sectional representation of tooth formation in white-handed gibbons, starting with the youngest in the top left and ending with the oldest in the bottom right. The first permanent tooth to form and emerge, M1, is highlighted along with the canine “C.”
In addition to characterizing ‘normal’ dental development, we also observed several developmental anomalies and pathologies in the sample. Our observations corroborate previous research showing that tooth formation generally proceeds ‘as scheduled’ despite various other disturbances to development.
It remains to be seen whether early development of the canine at the cost of delayed incisor formation is a pattern unique among all the apes, since most other studies of ape tooth formation have examined the lower jaw while our study focused on the upper jaws. But the canine-incisor tradeoff that we identified sets the stage for subsequent study of skull growth in this sample, as it highlights the many factors and functions that must be coordinated during growth.
While we have several projects planned with this unique dataset, we have also published the tooth formation data that we analyzed, and the original micro-CT scans themselves will be published to the online repository Morphosource.org soon, once a few more projects are finished.
Homo naledi is one of my favorite extinct humans, in part because its impressive fossil record provides rare insights into patterns and process of growth and development. When researchers began recovering naledi fossils from Rising Star Cave 10 years ago, one of the coolest finds was this nearly complete hand skeleton. The individual bones were still articulated practically as they were in life so we know which bones belong to which fingers, allowing us grasp how dextrous this ancient human was. And since finger proportions are established before birth during embryonic development, we can see if Homo naledi bodies were assembled in ways more like us or other apes.
The “Hand 1” skeleton of Homo naledi, adapted from a figure by Kivell and colleagues (2015). Left shows the palm-side view while the middle shows the back of the hand. The inset (b) shows many of the palm and finger bones as they were found in situ in Rising Star Cave.
In a paper hot off the press (here), I teamed up with Dr. Tracy Kivell to analyze finger lengths of Homo naledi from the perspective of developmental biology. On the one hand, repeating structures such as teeth or the bones of a finger must be coordinated in their development, and scientists way smarter than me have come up with mathematical models predicting the relative sizes of these structures (for instance, teeth, digits, and more). On the other hand, the relative lengths of the second and fourth digits (pointer and ring fingers, respectively) are influenced by exposure to sex hormones during a narrow window in embryonic development: this ‘digit ratio’ tends to differ between mammalian males and females, and between primate species with different social systems.
So, Tracy and I examined the lengths of the three bones within the second digit (PP2, IP2, DP2) and of the first segment of the second and fourth digits (2P:4P) in Homo naledi, compared to published data for living and fossil primates (here and here). What did we find out?
Summary of our paper showing the finger segments analyzed (left), and graphs of the main results (right). The position of Homo naledi is highlighted by the blue star in each graph.
The first graph above compares the relative length of the first and last segments of the pointer finger across humans, apes, and fossil species. The dashed line shows where the data points are predicted to fall based on a theoretical model of development. There is a general separation between humans and the apes reflecting the fact that humans have a relatively long distal segment, which is important for precise grips when manipulating small objects. Fossil apes from millions of years ago and the 4.4 million year old hominin Ardipithecus are more like apes, while Homo naledi and more recent hominins are more like modern humans. Because both humans and apes fall close to the model predictions, this means the theoretical model does a good job of explaining how fingers develop. Because humans and apes differ from one another, this suggests a subtle ‘tweak’ to embryonic development may underlie the evolution of a precision grip in the human lineage, and that it occurred between the appearance of Ardipithecus and Homo.
The second graph compares the ‘digit ratio’ of the pointer and ring fingers from a handful of fossils with published ratios for humans and the other apes. Importantly, the digit ratio is high in gibbons (Hylobates) which usually form monogamous pair bonds, while the great apes (Pongo, Gorilla, Pan) are characterized by greater aggression and mating competition and have correspondingly lower digit ratios. Ever the bad primates, humans fall in between these two extremes. Most fossil apes and hominins have digit ratios within the range of overlap between the ape and human ratios, but Homo naledi has the highest ratio of all fossil hominins known, just above the human average. It has previously been suggested that humans’ higher ratio compared to earlier hominins may result from natural selection favoring less aggression and more cooperation recently in our evolution. If we can really extrapolate from digit proportions to behavior, this could mean Homo naledi was also less aggressive. This is consistent with the absence of healed skull fractures in the vast cranial sample (such skull injuries are common in much of the rest of the human fossil record).
You can see the amazing articulated Homo naledi hand skeleton for yourself on Morphosource. Its completeness reveals how handy Homo naledi was 300,000 years ago, and it can even shed light on the evolution of growth and development (and possibly social behavior) in the human lineage.
I’m working on a project analyzing infant remains of Homo naledi, a species of human that lived in South Africa around 300,000 years ago. In order to paint a full picture of infancy in this species, we need to estimate how big (or small) naledi newborns were. But without fossil neonates that could provide direct evidence of body size at birth, this is a tricky task.
Ideally, we could simply use adult body size estimates for Homo naledi to predict its body size at birth, using the scaling relationship in other primates as a guide. For example, using an average adult body size of 44 kg for Homo naledi (Garvin et al., 2017) yields an estimated newborn size of around 1.5 kg, based on published primate dataset (Barton and Cappellini, 2011). But this approach necessarily overlooks variation within each species, not to mention variation and uncertainty in Homo naledi adult size. In addition, the 95% prediction interval for this estimate ranges from under 1 kg (smaller than an average baboon baby) to almost as large as a human neonate.
Primate body size scaling (Barton & Cappellini, 2011). The black line is the regression for catarrhines (purple squares and blue circles), and the shaded grey area is the 95% prediction interval for newborns at a given adult catarrhine size.
And this gets at the other issue with the regression-based approach to estimating newborn body size in fossil hominins: humans are bad at being primates in some ways, as illustrated here by the fact that we don’t fit the newborn-adult body size relationship that characterizes other catarrhines (apes and monkeys of Africa and Eurasia).
Humans give birth to collosal kids. In contrast, gorillas are the largest living primates as adults, but their newborns are only a little over half the size of human neonates. Why do we have such giant babies? The most proximate reason is that humans are born with adult-ape-sized brains and quite a bit of baby fat as far as mammals go (Kuzawa, 1998). This tells us how babies are big, but it still begs the ultimate question of why—an enduring puzzle that you may have read about in the New York Times last week.
In order to land on a reasonable estimate of newborn body size in extinct humans, we need to figure out when evolution blew up the kid. Unfortunately, the only fossil hominin neonates are two Neandertals from France and Russia dating to under 100,000 years ago—pretty remarkable, but they don’t necessarily tell us about earlier species like Homo naledi.
My colleague Jerry Desilva (2011) worked out a potential solution to this conundrum. He argued that one could work from adult brain size to newborn body size through the following steps. First, in contrast to newborn-adult body size scaling, humans are good catarrhines when it comes to newborn-adult brain size scaling. This means that we can reasonably estimate newborn brain size based on adult brain sizes, which are aplenty in the human fossil record. Second, humans and many other primate newborns have brains roughly 12% of their overall body mass, while the great ape newborns stand out with brains around 10% of their adult size. Putting these two pieces together, one could estimate newborn body size: Adult brain ➡️ newborn brain ➡️ 10–12% newborn body size
DeSilva showed that regardless of whether you use an ape or human model of newborn brain/body size, hominin babies from Australopithecus afarensis 3 million years ago onward were probably large relative to maternal body size, estimated independently using skeletal remains. It’s a bit of a tortuous approach to estimating body size at birth, but the assumptions are reasonable and it’s probably the best way to figure out this important life history variable given the fossil evidence. What does this mean for Homo naledi?
Virtual reconstruction of brain size and shape of the Homo naledi cranium “Neo” (work in progress). At 610 cm3, this is the largest and most complete Homo naledi endocast.
There are a few reliable adult brain size estimates for naledi, ranging from 465–610 cm3 (Berger et al., 2015; Garvin et al., 2017; Hawks et al., 2017), which based on catarrhine scaling would predict newborn brain size of around 170–210 cm3 (DeSilva and Lesnik, 2008). These brain sizes would then predict newborn body sizes of around 1.4–2.1 kg: the smol estimate is based on the smallest naledi adult brain size and a human model of newborn brain/body size; the chonk estimate is based on the largest naledi brain size and an ape brain/body model (pinkish stars in the boxplot below, left).
Boxplots of newborn body size in great apes. Gorilla, Chimpanzee, and Bonobo data from the Primate Aging Database(Kemnitz, 2019).
So, did Homo naledi have big babies? On the one hand, no: these 1.4–2.1 kg naledi newborns are outside the human range, and within the range of living great apes.
On the other hand, maybe Homo naledi babies were relatively large, though this depends on the size of Homo naledi adults. Recall from earlier that Garvin and colleagues arrived at an average estimated adult size of 44.2 kg. But this is an average of estimates for 20 separate naledi fossils, and each of these estimates has its own range of uncertainty. Garvin and team reported that the extremes of the prediction intervals for these estimates ranged from 28–62 kg. The second boxplot above shows newborn size relative to the adult average (sexes combined) for each species: for naledi, the six labels compare the smol and large newborn sizes (1.4 and 2.1 kg) with the adult average and extremes (28, 44, and 62 kg). Assuming the ‘true’ naledi sizes are somewhere in the middle of the range of estimates, naledi likely gave birth to babies 3–5% of adult body size, somewhat ‘intermediate’ between chimpanzees and humans (and bonobos…?) and similar to what DeSilva found for other hominins.
This is just a preliminary look at infancy in Homo naledi. There is a lot of uncertainty in these size estimates, but we should still be able to make some interesting inferences about growth and life history in our extinct evolutionary cousin.
REFERENCES
Barton, R. A., & Capellini, I. (2011). Maternal investment, life histories, and the costs of brain growth in mammals. Proceedings of the National Academy of Sciences, 108(15), 6169–6174. https://doi.org/10.1073/pnas.1019140108
Berger, L. R., Hawks, J., de Ruiter, D. J., Churchill, S. E., Schmid, P., Delezene, L. K., … Zipfel, B. (2015). Homo naledi, a new species of the genus Homo from the Dinaledi Chamber, South Africa. ELife, 4, e09560. https://doi.org/10.7554/eLife.09560
DeSilva, J. M. (2011). A shift toward birthing relatively large infants early in human evolution. Proceedings of the National Academy of Sciences, 108(3), 1022–1027. https://doi.org/10.1073/pnas.1003865108
DeSilva, J. M., & Lesnik, J. J. (2008). Brain size at birth throughout human evolution: A new method for estimating neonatal brain size in hominins. Journal of Human Evolution, 55(6), 1064–1074. https://doi.org/10.1016/j.jhevol.2008.07.008
Garvin, H. M., Elliott, M. C., Delezene, L. K., Hawks, J., Churchill, S. E., Berger, L. R., & Holliday, T. W. (2017). Body size, brain size, and sexual dimorphism in Homo naledi from the Dinaledi Chamber. Journal of Human Evolution, 111, 119–138. https://doi.org/10.1016/j.jhevol.2017.06.010
Hawks, J., Elliott, M., Schmid, P., Churchill, S. E., Ruiter, D. J. de, Roberts, E. M., … Berger, L. R. (2017). New fossil remains of Homo naledi from the Lesedi Chamber, South Africa. ELife, 6, e24232. https://doi.org/10.7554/eLife.24232
Kuzawa, C. W. (1998). Adipose tissue in human infancy and childhood: An evolutionary perspective. American Journal of Physical Anthropology, 107(S27), 177–209. https://doi.org/10.1002/(SICI)1096-8644(1998)107:27+<177::AID-AJPA7>3.0.CO;2-B
For last week’s AAPA conference, my friend and colleague David Pappano organized a workshop teaching about the many uses of the R programming language for biological anthropology (I’m listed as co-organizer, but really David did everything). After introducing the basics, we broke into small groups focusing on specific aspects of using R. I devised some lessons for basic statistics, writing functions, and resampling. Since each of the lessons could have easily taken up an hour and most people didn’t get to go through the activities fully, I’m posting up the R codes here for people to mess around with.
The basic stats lesson utilized Francis Galton’s height data for hundreds of families, courtesy of Dr. Ryan Raaum. To load in these data you just need to type into R: galton = read.csv(url(“http://bit.ly/galtondata“)). The code simply shows how to do basic statistics that are built into R, such as t-test and linear regression.
Some summary stats for the Galton data. The code is in blue and the output in black.
The lesson on functions and resampling was based on limb length data for apes, fossil hominins and modern humans (from Dr. Herman Pontzer). The csv file with the data can be downloaded from David’s website. R has lots of great built-in functions (see basic stats, above), and even if you’re looking to do something more than the basics, chances are you can find what you’re looking for in one of the myriad packages that researchers have developed and published over the years. But sometimes it’s necessary to write a function on your own, and with fossil samples you may find yourself needing to do resampling with a specific function or test statistic.
For example, you can ask whether a small sample of “anatomically modern” fossil humans (n=12) truly differs in femur length from a small sample of Neandertals (n=9). Traditional statistics require certain assumptions about the size and distribution of the data, which fossils fail to meet. Another way to ask the question is, “If the two groups come from the same distribution (e.g. population), would random samples of sizes n=12 and n=9 have so great an average difference as we see between the fossil samples?” A permutation test, shuffling the group membership of the fossils and then calculating the difference between the new “group” means, allows you to quickly and easily ask this question:
R code for a simple permutation test. The built-in function “sample()” is your best friend.
Although simply viewing the data suggests the two groups are different (boxplot on the left, below), the permutation test confirms that there is a very low probability of sampling so great a difference as is seen between the two fossil samples.
Left: Femur lengths of anatomically modern humans (AMH) and Neandertals. Right: distribution of resampled group differences. Dashed lines bracket 95% of the resampled distribution, and the red line is the observed difference between AMH and Neandertal femur lengths. Only about 1% of the resampled differences are as great as the observed fossil difference.
Here’s the code for the functions & resampling lesson. There are a bunch of examples of different resampling tests, way more than we possibly could’ve done in the brief time for the workshop. It’s posted here so you can wade through it yourself, it should keep you busy for a while if you’re new to R. Good luck!
These headlines, each saying something slightly different, are referring to a study by Indjeian and colleagues published in Cell. Researchers identified a stretch of DNA that is highly conserved across mammals, or in other words, it is very similar between very different organisms. In humans, however, this conserved region is actually missing (“hCONDEL.306”):
Fig. 4A from Indjeian et al. 2016. A stretch of DNA on Chromosome 8, “hCONDEL.306,” is very similar between chimpanzees, macaque monkeys, and mice, but is completely missing in humans (as is another stretch, hCONDEL.305).
That a stretch of DNA should be highly conserved across diverse animal groups suggests purifying natural selection has prevented any mutations from occurring here – alterations to this stretch of DNA negatively affected fitness. But that humans should be missing such a highly conserved region suggests that this deletion came under positive natural selection at some point in human evolution. This strategy, of seeking stretches of DNA that are similar between many animals but very different in humans, has led to the identification of hundreds of genetic underpinnings of human uniqueness. Some of these, such as the case in question, involve deleted sequences and have been termed “hCONDELs,” for “regions with high sequence conservation that are surprisingly deleted in humans” (McLean et al., 2011: 216). Others involve the accumulation of mutations where other animals show few or none (e.g., HACNS1; Prabhakar et al. 2008). In many (most?) cases these are “non-coding” sequences of DNA.
How can “non-coding” DNA help make humans upright?
As was predicted 30 years ago (King and Wilson, 1975), what makes humans different from other animals isn’t so much in the protein-coding DNA (the classical understanding of the term, “genes”), but rather in the control of these protein-coding genes. “Non-coding” means that a stretch of DNA may get transcribed into RNA but is not then translated into proteins. But even though these sequences themselves don’t become anything tangible, many are nevertheless critical in regulating gene expression – when, where and how much a gene gets used. It’s wild stuff. Indeed, “Many human accelerated regions are developmental [gene] enhancers” (Capra et al., 2013).
In the present case, hCONDEL.306 refers to the human-specific deletion of a developmental enhancer located near the GDF6 gene, which is a bone morphogenetic protein. The major finding of the paper, as stated succinctly in the Highlights title page, is that “Humans have lost a conserved regulatory element [hCONDEL.306] controlling GDF6 expression…. Mouse phenotypes suggest that [this] deletion is related to digit shortening in human feet.”
How do they link this “gene tweak” to digit shortening?
Since humans have lost this gene enhancer that is highly conserved in other mammals, Indjeian and team reasoned that the chimpanzee DNA sequence associated with this deletion, retaining the enhancer sequence, is likely the ancestral condition from which the human version evolved. They inserted the chimpanzee version into mouse embryos and watched what happened as they developed. The enhancer was only active in the mice’s back legs, specifically in the cartilage that would later become the lateral toe bones and cells that would become a muscle of the big toe (abductor hallucis). These are areas where humans and chimpanzees differ: our lateral toes are shorter than chimps’, and we only have one abductor hallucis muscle whereas chimpanzees have an additional, longer abductor hallucis (Aiello and Dean, 2002). So, we’re on our way to seeing how hCONDEL.306 might relate to our big toe or upright walking, as the headlines say.
But this still doesn’t explain how this deletion affects GDF6 gene expression, and therefore what this does for our feet. Pressing onward, the scientists compared the size of certain bones in mice with a normal Gdf6 gene, and those in which the Gdf6 gene was completely turned off (or “knocked out”). The Gdf6 knock-out mice had shorter lateral toe bones than regular mice, but they also had shorter big toes as well – the previous experiment staining mouse embryos showed the ancestral enhancer was expressed more in the latter toes, not so much the big toe.
Figures 5-6 from Indjeian et al. (2016) sum up the findings. Figure 5 (left) shows that the ancestral version of the GDF6 enhancer (blue staining) is most strongly expressed in the lower half of the body, especially the fifth toe bone. Figure 6 (right) shows that a lack of Gdf6 expression (black bars) results in shorter skull and toe bones. Combining these findings, humans lack a gene enhancer associated with the development of long lateral toes.
hCONDEL.306 doesn’t completely turn off GDF6, so this second experiment doesn’t really tell us exactly what the hCONDEL does. But the results are highly suggestive. Indjeian and team showed that Gdf6 affects toe length, among other skeletal traits, in mice. The ancestral enhancer that humans are missing seems to affect GDF6 activity in the leg/foot only. This illustrates a mechanism of modularity – as the authors state, “Loss of this enhancer would thus preserve normal GDF6 functions in the skull and forelimbs, while confining any … changes to the posterior digits of the hindlimb.” In other words, developmental enhancers allow different parts of the body to evolve independently despite being made by some of the same genes (such as GDF6).
As with any good study, results are intriguing but they raise more questions for future studies. The researchers conducted two experiments to investigate the function of hCONDEL.306: first putting the chimp version in mouse embryos to see where the ancestral enhancer is expressed, and then turning off Gdf6 completely in mice to see what happens. A more direct way to see what hCONDEL.306 does might be to put a longer stretch of the human sequence surrounding GDF6 containing (or rather missing) the ancestral enhancer into mouse embryos. I’m not a molecular biologist so maybe this isn’t possible. But this is important because the ancestral (chimpanzee) enhancer appeared to be most strongly expressed in the little toe, but of course this isn’t our only toe that is short compared to chimps. Similarly, how hCONDEL.306 relates to the abductor hallucis muscle remains in question – does it reduce the size of the intrinsic muscle present in both humans and chimps, or does it prevent development of the longer muscle that chimps have but we lack? We can expect to find hCONDEL.306 in the genomes of Neandertals (and Denisovans?), since they also have short toes, but what would it mean if they retained the ancestral enhancer?
So how does this gene tweak help with upright walking?
This is a really cool paper with important implications for human evolution, but something seems to have been lost in translation between the paper and the headlines (the news pieces themselves are good, though). The upshot of the study is that humans lack a stretch of non-coding DNA, which in chimpanzees (or chimp-ified mice) promotes embryonic development of the lateral toes and a big toe muscle. This may be a genetic basis for at least some aspects of our unique feet that have evolved under natural selection for walking on two legs.
But the headlines misrepresent this result, with words like “led to,” “allowed,” and “caused,” especially when these are followed by “big toe” or “upright walking.” hCONDEL.306 doesn’t really have anything to the big toe bone itself, although it might relate to a muscle affecting our big toe. The only sense in which the “Gene tweak led to humans’ big toe” (first title above) is that hCONDEL.306 might be responsible for our short lateral toes, which make our first toe look big by comparison. The other headlines are misleading since we know from fossil evidence that hominins walked upright long before we have evidence for short toes:
These little piggies get none. Fourth toe bones of living apes and humans (left) and (probable) hominins from 3-5 million years ago (right). I did my best to get all images to scale.
“Epigenetic,” from the fourth article headline, is simply wrong. Modern day epigenetics is a field concerned with the chemical alterations to the structure of DNA. Even the broad concept of epigenetic as originally devised by Conrad Waddington was about how environments (cellular or outside the body) influence development.
It’s hard to fit all the important and interesting information from scientific papers into news headlines. Still, it would be good if headlines more accurately portrayed scientific findings, especially avoiding such definitive verbs as “caused.” Especially in the realm of biology, people should know that there’s a lot that we still don’t know, that there’s lots more important work left to be done.
References
Aiello and Dean, 2002. Human Evolutionary Anatomy. Academic Press.
Capra et al., 2013. Many human accelerated regions are developmental enhancers. Philosophical Transactions of the Royal Society B 368: 20130025.
Indjeian et al. 2016. Evolving new skeletal traits by cis-regulatory changes in bone morphogenetic proteins. Cell http://dx.doi.org/10.1016/j.cell.2015.12.007
King and Wilson, 1975. Evolution at two levels in humans and chimpanzees. Science 188: 107-116 DOI: 10.1126/science.1090005
McLean et al., 2011. Human-specific loss of regulatory DNA and the evolution of human-specific traits. Nature 471: 216-219.
Prabhakar et al., 2008. Human-specific gain of function in a developmental enhancer. Science 321: 1346-1350.
We’ve arrived at the Planet of the Apes, also known as the Miocene, in my “Bones, Stones and Genomes” course. The living apes are but a small remnant of what was a pretty successful radiation starting around 20 million years ago. There were so many apes that it can be a bit confusing for students, but it’s important for setting up the biological and ecological contexts of hominin origins.
Possible evolutionary relationships of myriad Miocene apes and subsequent hominins. From Harrison (2010)
This week also marks my students’ first lab assignment, analyzing CT scans of bones. Here, we looked at how we estimate body size in extinct animals, using the KUPRI database and the free CT analysis software InVesalius. Because some of the KUPRI primates have body masses recorded, students can examine the relationship between animals’ weight and skeletal dimensions. The purpose of the assignment is to help familiarize students with skeletal anatomy, CT data and principles of linear regression.
One of the KUPRI specimens, an old female gorilla, with known weight.
I selected a few specimens for students to examine. After students download the massive files, they can load them into InVesalius for analysis. This program allows students to easily identify bone versus other tissues, and to create a 3D surface rendering of a highlighted region (tissue) of interest.
A grivet, Chlorocebus aethiops, with bone highlighted in 2D sections and as a 3D model. This little guy weighs only 4 kg!
It’s pretty easy to take simple linear measurements (and angles), assuming students can get oriented within the skeleton and identify the features they need to measure. It can be a little tricky to measure a femur head if it’s still in the acetabulum (below). Luckily, InVesalius lets you take measurements on both 2D slices or the 3D volume.
Let’s measure that femur head diameter.
So students do this for a few specimens and enter the data into Excel, which can then easily plot the data and provide a regression equation. They then use this equation to estimate masses of the specimens – if there’s a good relationship between mass and skeletal measures, then the estimates should be close to the observed values. Students use their equation to predict body mass of some Miocene apes based on femur head diameter and femur midshaft diameter, noting how confident they feel in their estimates given how well their regression performed on the training dataset. They also compare their mass estimates to those using another equation generated by Christopher Ruff (2003).
It might be a little intense for students totally unfamiliar with apes, bones and CT scans, but it should be a good way for them to learn lots of concepts we’ll revisit over the semester.
Here’s the lab assignment, in case you want to use it in your own class: Lab 1-Miocene masses
Lawnchair Anthropology 