Saturday 14 September 2024
The fossil record vs. The dinosaur to bird narrative.
Fossil Friday: More Evidence That “Feathered Dinosaurs” Were Secondarily Flightless Birds
in one of my recent Fossil Friday articles (Bechly 2024) I elaborated on the neoflightless hypothesis by paleo-ornithologist Alan Feduccia, who convincingly argues that all those feathered bipedal “dinosaurs” are in fact not related to theropod dinosaurs at all but rather represent secondarily flightless birds. I also discussed new evidence that strongly supports this view. Indeed, Agnolin et al. (2019) already commented in their study on the dinosaur-bird transition:
In a ground-breaking proposal, Xu et al. (2011) hypothesized that Archaeopteryx was more nearly related to deinonychosaurians than to birds and that deinonychosaurs become secondarily flightless, a hypothesis previously envisaged by Paul (2002). This hypothesis was supported by a variety of more recent analyses (Godefroit et al., 2013a; Xu et al., 2015; Hu et al., 2018).
Yet Another Discovery
After my article was published (Bechly 2024), I stumbled upon yet another discovery that may lend additional support to Feduccia’s hypothesis:
Just about a decade ago, Godefroit et al. (2013b) described a new supposed theropod dinosaur from the Middle-Late Jurassic Tiaojishan Formation of Liaoning in China. With an estimated age of 160 million years it is 10 million years older than the famous Archaeopteryx. They named the new species Eosinopteryx brevipenna, because of its reduced plumage. The single known specimen (an artist’s depiction of the living animal is above, or see here for the fossil) represents a very well-preserved fossil and almost complete skeleton, which allowed scientists to identify the new taxon as a close relative of the feathered dinosaur Anchiornis.
But this generated a problem: the new dinosaur appeared to be nested deeply in the tree of feathered dinosaurs, so that its reduced plumage cannot be a primitive state but has to be a secondary reduction from a more complete set of feathers. Furthermore, the bone structures of the shoulder articulation showed that the animal was not capable of flapping its arms or wings. This is even more perplexing, as this case of reduced flight adaptations predates the famous missing link Archaeopteryx. Consequently, the press release to the new study (University of Southampton 2013) announced that this fossil “challenges bird evolution theory” and suggested “that the origin of flight was much more complex than previously thought.” The lead author, Dr. Gareth Dyke from the University of Southampton, is quoted with this remarkable admission: “This discovery sheds further doubt on the theory that the famous fossil Archaeopteryx — or “first bird” as it is sometimes referred to — was pivotal in the evolution of modern birds.”
Challenged by Other Evolutionists
Don’t hold your breath, though, waiting for textbooks to be updated accordingly, because this confounding result was quickly challenged by other evolutionist scientists. They claimed that the distinct features of Eosinopteryx could rather be based on variability of the plumage and incomplete preservation of the tail, so that it could even represent the very same species as Anchiornis huxleyi (Pei et al. 2017, Hu et al. 2018, Agnolin et al. 2019). But these studies partly disagreed on certain crucial issues, such as the question of whether the shorter tail in Eosinopteryx is complete and diagnostic (Pei et al. 2017) or not (Hu et al. 2018, Agnolin et al. 2019). Moreover, other experts had recorded further diagnostic differences between the skeletons of two taxa, such as anteriorly convex pubic shafts that are present in Anchiornis but absent in Eosinopteryx (Foth & Rauhut 2017), or the length and shape of the prefrontal and maxillary processes (Guo et al. 2018). Also the cladistic studies by Lefèvre et al. (2014), Guo et al. (2018), Hu et al. (2018), and Pei et al. (2020) did not recover Eosinopteryx as closest relative of Anchiornis, or even rejected the monophyly of Anchiornithidae. One could almost get the impression that the desire to explain away inconvenient results may have guided the interpretations of those scientists, who denied the distinctness of Eosinopteryx.
There are clearly open questions and it definitely looks like the common dino-to-bird narrative has been massively oversold to the public and represents a theory with numerous holes and problems.
References
Agnolin FL, Motta MJ, Brissón Egli F, Lo Coco G & Novas FE 2019. Paravian Phylogeny and the Dinosaur-Bird Transition: An Overview. Frontiers in Earth Science 6: 252, 1–28. DOI: https://doi.org/10.3389/feart.2018.00252
Bechly G 2024. Fossil Friday: New Study Confirms “Feathered Dinosaurs” Were Secondarily Flightless Birds. Evolution News April 5, 2024. https://evolutionnews.org/2024/04/fossil-friday-new-study-confirms-feathered-dinosaurs-were-secondarily-flightless-birds/
Foth C & Rauhut OWM 2017. Re-evaluation of the Haarlem Archaeopteryx and the radiation of maniraptoran theropod dinosaurs. BMC Evolutionary Biology 17: 236, 1–16. DOI: https://doi.org/10.1186/s12862-017-1076-y
Godefroit P, Cau A, Dong-Yu H, Escuillié F, Wenhao W & Dyke G 2013a. A Jurassic avialan dinosaur from China resolves the early phylogenetic history of birds. Nature 498(7454), 359–362. DOI: https://doi.org/10.1038/nature12168
Godefroit P, Demuynck H, Dyke G, Hu D, Escuillié F & Claeys P 2013b. Reduced plumage and flight ability of a new Jurassic paravian theropod from China. Nature Communications 4(1): 1394, 1–5. DOI: https://doi.org/10.1038/ncomms2389
Guo X, Xu L & Jia S 2018. Morphological and Phylogenetic Study Based on New Materials of Anchiornis huxleyi (Dinosauria, Theropoda) from Jianchang, Western Liaoning, China. Acta Geologica Sinica – English Edition 92(1), 1–15. DOI: https://doi.org/10.1111/1755-6724.13491
Hu D, Clarke JA, Eliason CM, Qiu R, Li Q, Shawkey MD, Zhao C, D’Alba L, Jiang J & Xu X 2018. A bony-crested Jurassic dinosaur with evidence of iridescent plumage highlights complexity in early paravian evolution. Nature Communications 9(1): 217, 1–12. DOI: https://doi.org/10.1038/s41467-017-02515-y
Lefèvre U, Hu D, Escuillié FO, Dyke G & Godefroit P 2014. A new long-tailed basal bird from the Lower Cretaceous of north-eastern China. Biological Journal of the Linnean Society 113(3), 790–804. DOI: https://doi.org/10.1111/bij.12343
Paul GS 2002. Dinosaurs of the Air: The Evolution and Loss of Flight in Dinosaurs and Birds. The John Hopkins University Press, Baltimore (MD), 472 pp.
Pei R, Li Q, Meng Q, Norell MA & Gao K-Q 2017. New Specimens of Anchiornis huxleyi (Theropoda: Paraves) from the Late Jurassic of Northeastern China. Bulletin of the American Museum of Natural History 411, 1–67. DOI: https://doi.org/10.1206/0003-0090-411.1.1
Pei R, Pittman M, Goloboff PA, Dececchi TA, Habib MB, Kaye TG, Larsson HCE, Norell MA, Brusatte SL & Xu X 2020. Potential for Powered Flight Neared by Most Close Avialan Relatives, but Few Crossed Its Thresholds. Current Biology 30(20), 4033–4046.e8. DOI: https://doi.org/10.1016/j.cub.2020.06.105
University of Southampton 2013. Discovery of ‘Bird-Dinosaur’ Eosinopteryx Challenges Bird Evolution Theory. SciTechDaily January 24, 2013. https://scitechdaily.com/discovery-of-bird-dinosaur-eosinopteryx-challenges-bird-evolution-theory/
Xu X, You H, Du K & Han F 2011. An Archaeopteryx-like theropod from China and the origin of Avialae. Nature 475(7357), 465–470. DOI: https://doi.org/10.1038/nature10288
Xu X, Zheng X, Sullivan C, Wang X, Xing L, Wang Y, Zhang X, O’Connor JK, Zhang F & Pan Y 2015. A bizarre Jurassic maniraptoran theropod with preserved evidence of membranous wings. Nature 521(7550), 70–73. DOI: https://doi.org/10.1038/nature14423
Our fingers point to design?
The Formation of Our Digits Points to a Process with Foresight
Have you ever wondered how our fingers and toes form during embryonic development? Our digits are, in fact, sculpted from a paddle-like structure in the embryo through the process of apoptosis — that is, programmed cell death. During early development, the hands and feet begin as solid, webbed structures. Through carefully controlled apoptosis, the tissue between them is eliminated, facilitating the separation of the digits. As one paper put it, “the role of apoptosis can be compared with the work of a stone sculptor who shapes stone by progressively chipping off small fragments of material from a crude block, eventually creating a form.”1 Apoptosis, of course, serves other important biological functions as well — such as eliminating old, damaged, or infected cells.
When cells die as a consequence of acute injury, they tend to swell and burst, releasing their contents into the surrounding tissue. This is known as necrosis, and it can result in an inflammatory response that can be damaging to the cells around them. Death by apoptosis, by contrast, is much cleaner. During apoptosis, the cytoskeleton breaks down and the nuclear envelope disassembles, and the genetic material is broken down into smaller fragments. The surface of the cell is modified such that it attracts macrophages that phagocytose (engulf) the cell before its contents can spill out into the environment and cause damage.
The process of apoptosis is tightly regulated by genetic and biochemical signals, ensuring that the correct number of cells die in the right areas. But how could such a developmental process involving programmed cell death evolve in a gradual, incremental fashion without any awareness of where the target is? This presents a significant obstacle to unguided evolutionary mechanisms. Here, I will give a brief overview of how this remarkable process is regulated and controlled.
Initiation of Apoptosis
The zones of undifferentiated cells between what will become the digits are called interdigital mesenchyme. It is here that apoptosis is initiated by signaling molecules. For example, bone morphogenetic proteins (BMPs) are secreted signaling molecules that are critical for inducing apoptosis in the cells of the interdigital spaces.2 Indeed, knocking out BMP molecules has been shown to result in webbed feet in chickens.3 BMPs are upregulated in the regions between the forming digits, resulting in cellular death and tissue regression.
These BMPs bind to receptors on the surface of target cells in the developing limb bud.4 This, in turn, activates intracellular SMAD proteins, which translocate to the nucleus and regulate the expression of pro-apoptotic and anti-apoptotic genes.5 For instance, pro-apoptotic genes such as Bax and Bak (discussed later) are upregulated. Anti-apoptotic genes, such as Bcl-2, are also downregulated. This facilitates cell death in areas where tissue needs to be removed.
The activity of BMPs is regulated by antagonists, such as Noggin, which binds directly to BMPs, forming a complex that inhibits them from interacting with their receptors. This ensures that apoptosis only occurs in the interdigital spaces, while preserving the cells that will form the digits.6
Executioner Caspases
A family of proteases called caspases comprise the molecular machinery responsible for apoptosis.7,8 These proteases are initially produced as inactive precursors known as procaspases. In response to apoptosis-inducing signals, they are activated. Executioner caspases are responsible for dismantling essential cellular proteins — these are themselves cleaved (and thereby activated) by initiator caspases. One executioner caspase targets for destruction the lamin proteins that comprise the nuclear lamina, resulting in its disintegration.9 This facilitates the entry of the nucleases into the nucleus where they degrade the cell’s DNA. Other targets of executioner caspases include the cytoskeleton10 and other critical cellular proteins.
Execution of the Death Program: The Intrinsic Pathway
There are two ways in which the cell’s death program can be initiated — the extrinsic and intrinsic pathways. The extrinsic pathway is initiated by external signals through the binding of ligands to death receptors on the cell surface. The intrinsic pathway is triggered by signals from within the cell itself. Since the intrinsic pathway is associated with digit formation, it will be my focus here.
In nucleated animal cells, inactive procaspases roam, waiting for a signal to activate the death program and kill the cell. Unsurprisingly, then, the activity of caspases must be very carefully controlled. This presents another conundrum for their origins — how could they arise without a mechanism in hand for holding them in check until required?
The Bcl2 family of proteins is responsible for regulating caspase activation.11 Some of these proteins promote activation of caspases and apoptosis, while others negatively regulate these processes. Two essential proteins for promoting cell death are Bax and Bak.12 These proteins trigger the release of cytochrome c from the mitochondria. Other Bcl2-family proteins sequester apoptosis by inhibiting Bax and Bak from releasing cytochrome c.13 Critical to a cell’s survival is the balance between the activities of the pro-apoptosis and anti-apoptosis Bcl2-family members.
Image credit: David Goodsell, CC BY 3.0 https://creativecommons.org/licenses/by/3.0, via Wikimedia Commons
Upon release of cytochrome c from the mitochondria, the cytochrome c molecules bind to Apaf-1 (apoptotic protease activating factor 1).14 Apaf-1 has a specific region called the WD40 repeat domain that interacts with cytochrome c.15,16This binding induces a conformational change in Apaf-1, which allows it to oligomerize. The Apaf-1 monomers thus assemble into a large heptameric complex called the apoptosome (shown in the figure above). This wheel-like structure serves as a scaffold for further recruitment of procaspase-9 molecules.17 Within the apoptosome, the proximity of multiple procaspase-9 molecules results in their autocleavage and activation.18 This induces a caspase cascade (involving the activation of downstream effector caspases, such as caspase-3 and caspased-7), ultimately resulting in programmed cell death.19
The Need for Foresight
We began by comparing the role of apoptosis in digit formation to a stone sculptor, chipping off tiny fragments from a block with a view towards ultimately creating a form. Of course, an actual stone sculptor has a vision of the final form — the ability to visualize a distant outcome. Conversely, a feature of natural selection is that it lacks foresight, or any awareness of complex end goals. How can a mindless evolutionary process select for a process of carefully regulated programmed cell death during development, without knowledge of the target? It would seem that any process capable of producing this mechanism would have to possess intelligence and foresight — characteristics uniquely associated with a conscious mind.
Notes
Suzanne M, Steller H. Shaping organisms with apoptosis. Cell Death Differ. 2013 May;20(5):669-75.
Storm EE, Kingsley DM. GDF5 coordinates bone and joint formation during digit development. Dev Biol. 1999 May 1;209(1):11-27.
Zou H, Niswander L. Requirement for BMP signaling in interdigital apoptosis and scale formation. Science. 1996 May 3;272(5262):738-41. doi: 10.1126/science.272.5262.738. PMID: 8614838.
Ovchinnikov DA, Selever J, Wang Y, Chen YT, Mishina Y, Martin JF, Behringer RR. BMP receptor type IA in limb bud mesenchyme regulates distal outgrowth and patterning. Dev Biol. 2006 Jul 1;295(1):103-15.
Gomez-Puerto MC, Iyengar PV, García de Vinuesa A, Ten Dijke P, Sanchez-Duffhues G. Bone morphogenetic protein receptor signal transduction in human disease. J Pathol. 2019 Jan;247(1):9-20.
Guha U, Gomes WA, Kobayashi T, Pestell RG, Kessler JA. In vivo evidence that BMP signaling is necessary for apoptosis in the mouse limb. Dev Biol. 2002 Sep 1;249(1):108-20.
McIlwain DR, Berger T, Mak TW. Caspase functions in cell death and disease. Cold Spring Harb Perspect Biol. 2013 Apr 1;5(4):a008656. Erratum in: Cold Spring Harb Perspect Biol. 2015 Apr 01;7(4):a026716..
Cohen GM. Caspases: the executioners of apoptosis. Biochem J. 1997 Aug 15;326 ( Pt 1)(Pt 1):1-16.
Gheyas R, Menko AS. The involvement of caspases in the process of nuclear removal during lens fiber cell differentiation. Cell Death Discov. 2023 Oct 21;9(1):386.
Vakifahmetoglu-Norberg H, Norberg E, Perdomo AB, Olsson M, Ciccosanti F, Orrenius S, Fimia GM, Piacentini M, Zhivotovsky B. Caspase-2 promotes cytoskeleton protein degradation during apoptotic cell death. Cell Death Dis. 2013 Dec 5;4(12):e940.Kale J, Osterlund EJ, Andrews DW. BCL-2 family proteins: changing partners in the dance towards death. Cell Death Differ.2018 Jan;25(1):65-80.
Westphal D, Kluck RM, Dewson G. Building blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosis. Cell Death Differ. 2014 Feb;21(2):196-205.
Dlugosz PJ, Billen LP, Annis MG, Zhu W, Zhang Z, Lin J, Leber B, Andrews DW. Bcl-2 changes conformation to inhibit Bax oligomerization. EMBO J. 2006 Jun 7;25(11):2287-96.
Kim HE, Du F, Fang M, Wang X. Formation of apoptosome is initiated by cytochrome c-induced dATP hydrolysis and subsequent nucleotide exchange on Apaf-1. Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17545-50.
Hu Y, Ding L, Spencer DM, Núñez G. WD-40 repeat region regulates Apaf-1 self-association and procaspase-9 activation. J Biol Chem. 1998 Dec 11;273(50):33489-94.
Shalaeva DN, Dibrova DV, Galperin MY, Mulkidjanian AY. Modeling of interaction between cytochrome c and the WD domains of Apaf-1: bifurcated salt bridges underlying apoptosome assembly. Biol Direct. 2015 May 27;10:29.
Yuan S, Yu X, Topf M, Ludtke SJ, Wang X, Akey CW. Structure of an apoptosome-procaspase-9 CARD complex. Structure. 2010 May 12;18(5):571-83.
Li Y, Zhou M, Hu Q, Bai XC, Huang W, Scheres SH, Shi Y. Mechanistic insights into caspase-9 activation by the structure of the apoptosome holoenzyme. Proc Natl Acad Sci U S A. 2017 Feb 14;114(7):1542-1547.
Li P, Nijhawan D, Budihardjo I, Srinivasula SM, Ahmad M, Alnemri ES, Wang X. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell. 1997 Nov 14;91(4):479-89.
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