Writing in Biology - Section 1

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.

The presymptomatic phase of kuru lasts, on average, 10 to 13 years but incubation time can range from 5 years to 50 years (Collinge et al., 2008). Mean clinical duration of the disease is 12 months with a range of 3 months to 2 years (Collinge et al., 2008). Kuru infection presents itself in three progressive stages: ambulatory, sedentary, and terminal (Alpers, 2005). The primary physical symptom of the disease, cerebellar ataxia, worsens as the disease advances through these three stages(Gajdusek, 1957). In the ambulatory phase, patients demonstrate a loss of muscular coordination though they are still capable of speaking and moving around (Gajdusek, 1957). In the sedentary stage, infected individuals show stronger ataxia that manifests as major dysarthria, frequent, excessive bursts of laughter and the impossibility of unassisted movement (Gajdusek, 1957). At the terminal stage, infected individuals can no longer sit without support, the ability to speak is lost, urinary and fecal incontinence is common, dysphagia begins, and many develop ulcerated wounds that are prone to infection (Gajdusek, 1957). Death occurs shortly thereafter either due to wound infection or terminal static bronchopneumonia (Gajdusek, 1957).

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

Climate change, specifically global warming, has been associated with increases in atmospheric CO₂ levels. Fixation of this airborne carbon dioxide and subsequent removal from the atmosphere is possible, though impractical due to little or no economic incentive. Hepburn et al. counter this position with viable utilization of captured CO₂ that yield decent economic return. Some of these utilities include chemicals (methanol, urea, plastics), fuels (methanol/methane), microalgae products (biofuels, biomass, aquaculture feed), and concrete and various building materials¹. In addition to these ventures, Hepburn et al. also lay out the probability of re-release of carbon dioxide from these various applications¹.

(1) Hepburn, C., Adlen, E., Beddington, J. et al. The technological and economic prospects for CO₂ utilization and removal. Nature 575, 87–97 (2019) doi:10.1038/s41586-019-1681-6

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

Embryosis is the formation of an embryo. There are two main steps to this process: blastulation, and gastrolation. The begining of this process is the sperm and egg cell fusion to form a zygote. This is when the genetic material merges and all cells are pluripotent. Next there is clevage, compaction, and differentiation forming the blastocyte. The overall size of the blastocyte is not much bigger than the zygote because of compaction. There are many more cells in the blastocyte because of clevage, and some differentiation between the inner cell mass and surrounding cells. Gastrolation is the formation of three distinct layers in the blastocyte which will differentiate. The top layer is the ectoderm, the middle layer is the mesoderm, and the bottom layer is the endoderm. The ectoderm differentiates into the nervous system and the skin. The mesoderm differentiates into the muscles; the endoderm differentiates into the internal organs. This process is virtually the same for all mamals. The outcome is very different because of the genetic information fused, resulting in a wide range of organisms.

Dio lox sites are double inverted orientation lox sites. This is a mechanism used by neurobiologists to insert different genes intot the brain of model organisms. The lox sites surround a gene that you want to insert. The gene is in nonsense orientation, meaning it will not be expressed unless it is in the presence of CRE recombinase which is able to flip the gene in certain circumstances. If there are dio lox sites (in the presence of CRE recombinase), then this is a two step process to perminantly flip the transgene into the sense direction to be expressed. The first step is one set of lox sites are brought togehter by the CRE recombinase. One of the lox sites the CRE is acting on will be inserted to the other side of the transgene and the transgene will be flipped. This leaves three lox sites on one side of the transgene, and one lox site on the other side. Of the tree lox sites on one side, two are in a pair and facing the same direction. These lox site pairs, in the presense of CRE will be spliced out of the gene sequence. The splicing of the lox sites from the gene sequence leaves two lox sites from different pairs in each sequence of DNA (one splices, and one with the transgene). Ultimately, this is a perminant change to the DNA because lox sites from different pairs cannot work together, the CRE will not recognize them as a pair. Therefore, the perminant flip will allow for the expression of the transgene in the cells that express CRE recombinase.