Handrigan, G. R. (2003). Concordia discors: duality in the origin of the vertebrate tail. Journal of Anatomy, 202(3), 255–267. doi: 10.1046/j.1469-7580.2003.00163.x
Tail formation stemming from ventral ectodermal ridge (VER) activity is not like that of AER. VER does not employ FGF signaling, and is therefore an entirely different system. Presents the idea that tails form similar to that of a limb bud (secondary development) as well as the view of gastrulation
Interdigital webbing is found among many vertebrates in the early stages of development. However, many of these organisms remove this webbing through tissue-specific apoptosis, removing the interdigital membrane back towards the digits. Some mammals retain this webbing, such as bats. This is feasible through inhibition of apoptosis, specifically through the BMP inhibitor Gremlin.1 BMP signaling typically results in apoptosis in expressed tissues, but through Gre inhibition, these tissues remain and can be repurposed-in the case of bats-for flight.
(1) Weatherbee, S. D., Behringer, R. R., Rasweiler, J. J., & Niswander, L. A. (2006). Interdigital webbing retention in bat wings illustrates genetic changes underlying amniote limb diversification. Proceedings of the National Academy of Sciences, 103(41), 15103–15107. doi: 10.1073/pnas.0604934103
In the developing tooth, enamel deposition varies among organisms. In omnivorous homo sapiens, enamel strength and quantity is much less than that of a sea otter, who prodominantly feeds on hard shellfish. It is important, then, to understand this pathway that results in this differential deposition of enamel in developing teeth. Stem cells in the developing teeth that express Sox2 travel to the inner enamel epithelium within the developing tooth1. There, they give rise to transit amplifying (TA) cells that rapidly divide, move to the distal tip of the developing tooth, and differentiate into ameloblasts1. Ameloblasts deposit enamel matrix proteins. As a result, Sox2 overexpression could lead to increased enamel deposition and a hardening of teeth.
(1) Li, J., Parada, C., & Chai, Y. (2017). Cellular and molecular mechanisms of tooth root development. Development, 144(3), 374–384. doi: 10.1242/dev.137216
(excerpt from evo-devo creative writing essay)
In order to combat cold waters as well as the cold Eurasian winters, Homo lontra regained the full-coverage body hair previously lost in many hominid species. This loss of body hair is a well-documented phenomenon in developmental biology, and has been traced to inactivation of specific hair keratins. Keratins are an integral structural element of many epithelial appendages, such as hair, nails, and skin. Mutations to keratins can result in very clear diseased phenotypes in humans, such as complete alopecia or pseudofolliculitis barbae.4 It is probable, then, that a loss of function in a keratin gene may have led to the evolution of no body hair in hominid populations, and a gain of function of these now-pseudogenes may allow for the re-evolution of full body hair.
Alcohol-related liver disease can result in alcoholic hepatitis, a diseased and inflamed state of the liver. In mice, the gut microbiome produces toxins that contribute to liver damage in response to ethanol. Duan et al. identified a two-unit exotoxin cytolysin, excreted by Enterococcus faecalis as a cause of injury to the liver1. In patients with alcohol-related liver disease, Duan et al. also found increased numbers of E. faecalis in these patients' microbiomes1. Analyzing this further, Duan et al. used E. faecalis targeting bacteriophages in humanized mice with ethanol-induced liver disease1. They found that through this treatment, ethanol-induced liver disease was abolished in these test subjects, though more comprehensive testing must be performed to determine the true efficacy of this treatment.
(1) Duan, Y., Llorente, C., Lang, S. et al. Bacteriophage targeting of gut bacterium attenuates alcoholic liver disease. Nature (2019) doi:10.1038/s41586-019-1742-x
Weatherbee, S. D., Behringer, R. R., Rasweiler, J. J., & Niswander, L. A. (2006). Interdigital webbing retention in bat wings illustrates genetic changes underlying amniote limb diversification. Proceedings of the National Academy of Sciences, 103(41), 15103–15107. doi: 10.1073/pnas.0604934103
Pajni-Underwood, S., Wilson, C. P., Elder, C., Mishina, Y., & Lewandoski, M. (2007). BMP signals control limb bud interdigital programmed cell death by regulating FGF signaling. Development, 134(12), 2359–2368. doi: 10.1242/dev.001677
MSX2 inhibits the promoter sequence of amelogenin, antagonizing downstream C/EBPα as well as DLX2. This pathway is illustrated in figure 1. In the heterozygous mutant, decreased transcriptional repressor activity of MSX2 ultimately results in increased amelogenin expression.2 This increase of expressed amelogenin in the developing tooth ultimately results in increased enamel thickness, as well as increased rod size.2 In figure 2, Molla et al. analyzed 3 month postnatal mice with the wild type, heterozygous, and homozygous mutations. Molla et al. measured a 1.3-fold increase in enamel thickness2 in Msx2+/- mutants compared to the wild type. Of course, this Msx2+/– mutation is not a reliably heritable trait, and therefore a consistent observation of this phenotype among Homo Lontra populations must be the result of a cis-regulatory mutation, specifically within MSX2 enhancers. MSX2 contains a BMP-responsive enhancer sequence3, and a subsequent mutation within this enhancer sequence in Homo Lontra was found to result in the similar phenotype to Msx2+/– mutants.
(Adapted from Developmental Biology essay)
Homo Lontra is a species of hominid located in modern day coastal Europe. Upon increased competition from the Homo Sapien invasion of Eurasia due to their emigration out of Africa, Homo Neanderthalensis was forced to the coast, outcompeted for access to many land animals and foraging areas. There, Homo Lontra evolved from Neanderthals, with visible adaptions for a diet of coastal marine foraging. This included webbed feet for better aquatic propulsion, a hardened enamel for consuming hard-shelled marine animals, and the re-evolution of dense body hair to protect their bodies from the cold European winters and water. These traits are similar to those of other aquatic mammals-such as otters (Homo Lontra’s namesake)-but a complete molecular and developmental analysis must be performed in order to determine their true origins.
The teeth of Homo Lontra are much tougher than that of Homo Sapiens due to their increased enamel thickness. In mice and humans, the teeth are not continuously grown or renewed after development; therefore, any alteration to tooth structure would have to take place developmentally.1 Muscle segment homeobox 2 (MSX2) encoded proteins act as repressors; specifically affecting epithelial-mesenchyme interactions as well as ameloblast differentiation, a cell that deposits enamel proteins during tooth development.2Msx2+/– mutants display stronger expression of amelogenin (proteins related in amelogenesis; enamel development) than that of Msx2+/+ individuals, with the heterozygote displaying a twofold increase in amelogenin expression.2
In the developing tooth, enamel deposition varies among organisms. In omnivorous homo sapiens, enamel strength and quantity is much less than that of a sea otter, who prodominantly feeds on hard shellfish. It is important, then, to understand this pathway that results in this differential deposition of enamel in developing teeth. Stem cells in the developing teeth that express Sox2 travel to the inner enamel epithelium within the developing tooth1. There, they give rise to transit amplifying (TA) cells that rapidly divide, move to the distal tip of the developing tooth, and differentiate into ameloblasts1. Ameloblasts deposit enamel matrix proteins. As a result, Sox2 overexpression could lead to increased enamel deposition and a hardening of teeth.
(1) Li, J., Parada, C., & Chai, Y. (2017). Cellular and molecular mechanisms of tooth root development. Development, 144(3), 374–384. doi: 10.1242/dev.137216
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