Drafts

To determine if there are different sized trees in different habitats we measure the diameter at breast height (dbh) of trees on a north facing slope, south facing slope and a flat. Each location was at the Mount Holyoke Range in Amherst, Massachusetts. Each site differed in steepness and direction of slope, but not longitude of latitude. The sites were located near a point on the ridge referred to as “The Notch.” This location is also where highway 116 crosses the notch. At each site, the dbh (measured to the nearest 0.1cm), and the species of each live adult tree was measured.

Flight is one of the most involved adaptations an organism can have. What that means is that when an organism is on the evolutionary path to flight, everything else about that organism's morphology/lifestyle must change to accommodate the ability to fly. The bones must become lightweight, and habitat is most likely at a high altitude. Organisms evolving for flight have to make themselves as light as possible, meaning that heavy feathers are not a good option. The body must become streamlined in order to get the best possible flying efficiency, or face losing energy to fight additional air resistance from a non-aerodynamic body. Flying has only evolved once in mammals: the bat. The bat has a lightweight skeleton with long, thin arms that provide the framework for their wingspan. Unlike most flying animals, their eyesight can actually be very poor, and some species of bats rely on echolocation to fly around and locate prey. Flying is an all-in, evolutionary commitment, and a lifestyle that has been lived out successfully by many thousands of animals.

The steepness of a slope is an abiotic factor of the microclimate and habitat of that area. Slope aspects such as potential energy income can differ between steeper and less steep slopes (Méndez, Meave, Zermeño, Ibarra, Woods, 2016). Significant difference between individual sizes of vegetation can be found on different slopes. Although this can be due to the south facing slopes getting higher incidence of solar radiation, it could also be due to the potential energy income of larger trees on a slope versus smaller trees. If this is the case then both north and south facing slopes should have smaller trees if the slope is steeper. The larger trees of the same species are generally older than the smaller trees of the same species and this can idea can help make an inference on mortality rates of a species if there are more small trees in a given area than large ones.

The overall objective of our proposal is to create a phylogenetic tree to determine the reliability of HOXC genes as an indicator of phylogeny. By aligning the sequence, the genes will become easy to compare and allow for the creation of a phylogenetic tree, as proposed. The sequencing data can also be used to determine how conserved the HOXC gene is. By understanding the evolutionary and genetic differences of HOXC genes between different species, the function of HOXC genes, which are currently unknown, can be better understood. The creation of a phylogenetic tree will allow for the determination of reliability of using HOXC genes as an indicator of phylogeny. If the phylogenetic tree proves to be reliable, this would be a phylogenetic tree of vertebrates that can be used in order to trace the evolutionary history of vertebrates. If new species were to be found, its HOXC gene can be sequenced to determine its phylogeny accurately.

When an embryo is 2 weeks old, the heart muscles know their fate and they rearrange themselves in a crescent shape. Cells go to specific places and act as progenitors to form different parts like the atria, ventricles. By the third week, a tube forms that starts beating that later becomes the right ventricle. Other cells become the left ventricle. As time goes by the cells become more specific in terms of location. Newborns usually present problem only in a localized area, example, they could be born with all the chambers completely intact, but missing the right ventricle. They must have had a mutation in the cells responsible for the right ventricle that caused such a phenotype. Animal models such as chick, mouse, zebrafish embryos etc have been used to understand this process on a molecular level. However, animal models were difficult to study for very early stages. Thus, induced pluripotent stem cells became handy in order to study such preliminary phases. These cells mimic the cardiomyocytes in vivo. Together with stem cells in a dish and animal models, it was possible to understand the gene networks that chalk out the map for cardiac fate. His team was able to figure out the key components in the gene network: the Notch1, Gata4, Tbx5, Nkx2.5 and Ptnp11 are genes that are responsible for the creation of the chambers. Heterozygous mutations (mutation of a single allele) in these genes can cause the defect. It is not necessary for the mutation to be a loss of function mutation; even when the dosage of the gene was reduced, they observed the same phenotype. So this suggested that by raising the dosage of the genes, it would be possible to reverse the defect. 

When cells lose water, many problems arise. Cellular membranes are made of a lipid bilayer that is extremely hydrophobic. This membrane requires the presence of water to stay together because the polarity surrounding the lipids keeps their organization favored by entropy and forces all the hydrophobic tails together. When water loss occurs, the cell membranes disintegrate, among other problems that arise. One mechanism in nature that exists to prevent this during periods of drought in plants. In order to prevent these effects, the plant cells produce a molecule that performs that same function that water was serving. These clever molecules are simple sugars that have hydrophilic properties and are able to keep cell membranes together and working correctly. These sugars include sucrose, raffinose, stachyose and trehalose. It has been found that these same sugars are able to prevent protein aggregation with water loss as well. These sugars can also be added in excess to cells to allow researchers to freeze down cells for later use over very long periods of time, for example 50 years. 

At the earliest stage of life, we are just small fertilized eggs called zygotes. These zygotes are just balls of cells that keep dividing to form an embryo. After the cells undergo some rearrangement and each cell has a future to look forward to, they start working towards making the specific organs. When it comes to our limbs, something similar happens. Molecules called morphogens help by forming our arms and the position of each part depends on how much or how little of the molecule is present from one end to another. Once we have our arms, we get more in depth into forming our digits – our fingers! We have genes called the Hox genes – in short, they are responsible for making the decision of which body part ends up where. They are also in charge of deciding on our fingers – the numbers, the length between the fingers. The expression of Hox 13 and Gli3 genes are possibly the most important in order to determine those aspects. So what happens when we stop the genes from working? We create mutants. When the Gli3, Hox 11-13 and Hox 13 genes are on we get normal fingered hands. When we alter the Hox 13 genes or prevent the Hox 11-13 from expressing, there is significant reduction in the gaps between our fingers. Taking this a little further, we turn off the Gli3 genes from expressing, we get more than five fingers. The fingers also end up with our fingers being completely joined from the top. The fingers and the gaps can be seen as waves. The peaks of the waves can be seen as the fingers and the gaps can be seen as the drops in the waves. Thus the length between the fingers can be called wavelengths. So as the Hox genes are turned off, the wavelength reduces.

Pigmentation in dogs and other mammals (including you) is caused by the relative amounts and types of two classes of pigment: eumelanin and phaeomelanin. The eumelanins are the black and brown pigments, and the phaeomelanins are red and yellow. Both eumelanins and phaeomelanins are synthesized in pigment-producing cells called melanocytes. First, the enzyme tyrosinase converts the amino acid tyrosine to a chemical called dopaquinone. If the enzyme called tyrosinase-related protein 2 (TRP-2) is present, it converts the dopaquinone to a version of eumelanin that has a brown color, Cocoa's pigment. If the enzyme called tyrosinase-related protein 1 (TRP-1) is present, it converts the brown version of eumelanin into the final, black pigment.

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