My trip in Salt Lake City, Utah, continues this week and I have more photos to share, exploring reptilian, dinosaur, and mammalian evolutions. Following our trip to the Natural History Museum, we visited the Museum of Ancient Life at Thanksgiving Point. Though the building looks like a dino-decorated movie theater from the outside, inside it actually has an impressive collection of fossils and replicas. (In fact, it actually has more specimens on display than the NHM.) So here is a visual tour through Utah’s Museum of Ancient Life.
Eryops, an early transition amphibian that lived about 295 million years ago.
Dimetrodon, a large synapsid reptile that went extinct about 40 million years before the earliest dinosaurs arose.
Herrerasaurus, one of the earliest known dinosaurs, named for the rancher who discovered it.
Othnielia, a tiny ornithischian dinosaur.
Goniopholis, an ancient (and modestly-sized) crocodile.
A Camarasaurus skull, a herbivore that is the most common of the sauropods found in North America.
Ceratosaurus, standing over a Camarasaurus carcass. It’s name means “horned lizard”, for the small horn above its nose. It lived during the late Jurassic period.
Hesperosaurus, a type of stegasaur who lived about 156 million years ago.
Camptosaurus, a herbivore that lived during the Late Jurassic period.
Tanycolagreus topwilsoni, a theropod from the Late Jurassic in North America. The primary representative specimen of the species is held at the Museum of Ancient Life.
Utahraptor, a theropod dinosaur, the largest of the family Dromaeosauridae. It lived during the early Cretaceous period.
Tylosaurus proriger, the largest of the marine reptilian mososaurs at up to 50 feet in length.
Archelon ischyros, the largest turtle to have ever lived.
An extinct species of pygmy elephant that died out only about 10,000 years ago.
Well, that concludes my tour of the Museum of Ancient Life in Salt Lake City, Utah. I highly recommend a visit to this and the NHM if you stop by Salt Lake. There are plenty more specimens on display I haven’t shown here. This was just to wet your whistle. 😉 Hope you’ve enjoyed the tour.
I had a toy plastic Dimetrodon as a kid. That big fan like thing on its back might have had some kind of cooling function. Sure wish that it would be possible to time travel just to see some of those beasts in action.
Yeah, wouldn’t that be awesome? 😀 (Of course, if we could observe from a safe distance!)
Sounds like a fun vacation/conference. How did your presentations go, any links to your abstracts? When I lived in NYC I would go at least once a year to the Museum of Natural History, could never get enough.
Not really sure where to find links for abstracts on IMFAR, but I’ll just post them here…
Robert, here’s the poster abstract:
Autism-risk, Schizophrenia-risk, and Central Nervous System-related Genes Display Genomic Features Common to Genes of Developmental Regulation
Background: A large subset of genes in the human genome are involved in regulation of developmental processes. These include functional subsets like chromatin remodelers, transcription factors, translational regulators, and intracellular signaling transducers. Such genes typically contain large introns, produce longer more complex proteins, and preference retention of transposable element (TE) insertion into intronic sequences over time for reasons not entirely understood. Each of these features is related to the general functions of these developmental genes. A previous study of ours reported higher absolute TE content in autism-risk genes (Williams et al., 2013). In addition, King et al. (2013) reported preliminary findings of longer gene size in risk genes. Therefore, in this study we investigate whether autism (ASD)-risk, schizophrenia (SZ)-risk, and central nervous system (CNS)-related genes share features with genes of general developmental regulation, so that we may better understand the functions and mutational trends of our genes of interest. Objective: Using whole genome control (WGC) for comparison, we determined whether ASD-risk, SZ-risk, and CNS-related genes are enriched in TEs, are longer, and code for larger proteins. Housekeeping (HK) genes are used as a comparison group due to their compactness. Methods: All known protein-coding genes were acquired from RefSeq to compile the WGC. Autism genes with 10+ rating were downloaded from AutismKB database (N = 451). SZ-risk genes were acquired from SzGene database (N = 38). CNS genes were taken from the human Neurogenesis and Neural Stem Cell (PAMM-404) PCR array from Qiagen to be used as a representative sample (N = 85). Human HK genes were taken from Eisenberg and Levanon (2003) (N = 565). TE content was acquired on human genome 18 from the TranspoGene database and data on gene and protein lengths from NCBI RefSeq. TE analysis was performed using a negative binomial regression, meanwhile a gamma regression was used for assessing gene and protein lengths. Results: All groups significantly varied from WGC in terms of intronic TE content; meanwhile, there were no significant differences in non-intronic (promoter, exonic, exonized) content in experimental groups versus control, with the exception of the HK genes, which displayed significantly greater numbers of exonized TEs and fewer exonic elements (p-values < 0.001). Gene length varied significantly across all groups: ASD, SZ, and CNS gene groups were significantly longer in length than WGC, while HK genes exhibited the opposite trend (p-values < 0.001). Protein lengths followed similar trends as gene length across groups, with the exception of the SZ gene group, whose protein lengths did not vary compared to WGC in spite of having the largest gene length average. Conclusions: ASD-risk, SZ-risk, and CNS-related genes house considerable TE content, and are larger; meanwhile, ASD and CNS genes produce larger protein products as compared to WGC. On the other hand, HK genes, known for their overall compactness and small intronic sizes, exhibit opposite trends as seen in the other experimental gene groups. These results suggest that ASD-risk, SZ-risk, and CNS-related genes may be classed with developmental regulatory genes and, as such, likely follow functional and mutational trends in this large subset of mammalian genes.
And here’s the panel. I also included some of our current data which wasn’t spoken about in the original submission, involving genetics results on forms of intellectual disability with highly comorbid autism. I also talked about the current field’s obsession with the synapse and how the data suggests we should really broaden our focus to all stages of neuronal development.
Genetics Studies Indicate that Disturbances in Premigratory Neuroblast Maturation Are Core Features in the Neuropathology of Autism
Background: Neuropathological studies of autism report cortical and subcortical malformations in the vast majority of cases, indicating early disturbances to neurogenesis and neuronal fate determination. Genetics research, however, has largely focused their efforts on understanding synaptopathology in the condition. This places the two fields at odds with one another, making it a challenge to integrate the research coming from these disparate disciplines. Objective: To address whether high-risk autism gene products affect multiple stages of neuronal development, from neurogenesis and induction, to neurite extension and synaptogenesis, in the hopes of reconciling the range of findings reported in autism. Methods: Because many studies have relied on simplified Gene Ontology (GO) terms to investigate overlapping biological functions in autism-risk genes, we instead took a more direct approach to understand the various functions that these gene products maintain and what stages of neuronal development are ultimately affected. We did so by scouring the original literature upon which GO terminology has been founded, searching for indications of involvement in neurogenesis and pre-migratory neuronal fate determination. We investigated 197 high-risk syndromic and nonsyndromic autism genes, derived from the SFARI and AutismKB databases, hereto referred as the “core set”. A 0-3 rating scale was used to summarize findings for each gene: “0” indicated that there was no known relationship between the gene product and early neuroblast development, “1” suggested minor evidence, “2” indicated moderate, highly-suggestive evidence for involvement, and “3” indicated a confirmed direct relationship. We also looked for evidence as to whether these same gene products influenced later stages of neuronal development, specifically in neurite elongation, branching, synaptogenesis, and plasticity. Results: Our review revealed that 88% of the core set attained a rating of 2-3, with 52% of the core gene set directly influencing induction and/or pre-migratory neuroblast differentiation. This was most frequently manifest as premature or delayed neurogenesis in loss-of-function and overexpression studies. Meanwhile, 80% of the core set gene products also influenced later stages of neuronal development, e.g., neuritogenesis and synaptogenesis. Conclusion Most high-risk autism gene products influence multiple stages of neuronal development, encompassing induction and neurogenesis, pre-migratory differentiation, migration, axonal and dendritic elongation and branching, synapse formation, and dendritic and synaptic plasticity. This may be due to a combination of cascading effects from earlier foundational stages leading to a reverberation throughout the life of the neuron, as well as functional redundancy of gene products that are reused at multiple stages of neuronal development. This work offers a theoretical construct in which to view the neuropathological and genetics research produced on autism to date under a single umbrella, one which helps to integrate apparently disparate findings into a single pathological concept.
Thanks, very interesting.Remember our discussion of Klinefelter syndrome a while ago? The C-BASS (Chinese Benzene Sperm Study group) is a collaboration between NIH and Chinese researchers. They have a study that shows workers exposed to Benzene in Chinese manufacturing plants have increased rates of sperm aneuploidy including the production of XY sperm which leads to the Klinefelter 47, XXY mutation at conception. While the origins of de novo XXY mutations is not known, this study provides a direct causation link for the first time for Klinefelter syndrome:
Sperm aneuploidy can result in several combinations (XY, YY and XX) that at conception when combined with one X chromosome from the mother will result in 47, XXY (Klinefelter syndrome) 47, XYY (XYY syndrome) and 47, XXX (Triple X syndrome). All three are associated with abnormal developmental disabilities and all three have high rates Autism.
That’s very interesting, I wasn’t aware of that. I’ll have to remember that in future.