Drafts

          The debate over nature vs nurture has been going on for at least hundreds of years, and our modern understanding of DNA and the research around behavioral genetics is just another facet of that discussion. We already know human responses to various stimuli are triggered by numerous neurochemicals and molecular signalling pathways, which are in turn regulated by the activation and deactivation of particular genes. The way that I’ve always understood it, though, is that while there are certain sets of genes that, if inherited, may predispose you to be more susceptible to addiction or obesity or whatever else, it is not in any way guarantee that you’ll actually exhibit these traits. In addition, the field of epigenetics has also revealed that environmental factors can impact when and how a gene is activated or deactivated. For instance, in the article by Kathleen Mcauliffe, Jaroslav Flegr’s research into T. gondii did not illustrate human genes driving disordered behavior, but rather external environmental factors which were, in this case, the presence and disruptive influence of the T. gondii parasite. As discussed in Amy Harmon’s article “The DNA Age”, some people see themselves as “hostages” to their genes. I disagree with this attitude, excluding in cases of diagnosed disorders, because I believe it overstates how much individual genes can direct complex and variable human behaviors. I personally think of it as DNA acting as a foundation for what might be possible, and then factors from both the physical environment and the social environment build up from there and result in the formation of what behavioral tendencies are exhibited.

This article is titled “Inhibition of the substantia nigra pars reticulata produces divergent effects on sensorimotor gating in rats and monkeys.”  It piqued my interest because I am a part of Karine Fenelon’s lab here on campus, in which we investigate the neural circuits that modulate sensorimotor gating.  In the study, the GABA_A receptor agonist muscimol was used to test the role of the SNpr in auditory pre-pulse inhibition (PPI), a key component of sensorimotor gating.  From class, we know that GABA is the major inhibitory amino acid neurotransmitter, so muscimol must mimic its inhibitory effects on target neurons.  In the study, it was found that the inhibition of the SNpr using muscimol disrupted PPI in rats, while facilitated PPI in rhesus macaques.  This study discovered these divergent effects.  I wonder what differences in neuron connections contribute to this divergence, because there must be a difference either upstream or downstream of the point of innervation of the SNpr.  I also wonder what the effect of muscimol on the SNpr in mice is, since this is the model organism we use in lab.

https://www.nature.com/articles/s41598-018-27577-w.pdf

            Patient 3 has Fibrodysplasia Ossificans Progressiva. Patients with this disease have abnormal development of bone in parts of the body where bone is not typically present. The mode of inheritance is autosomal dominant. It is caused by a gene called ACVR1. The ACVR1 protein receptor is found in skeletal muscle and cartilage and regulates ossification. In this disease, the mutated ACVR1 protein is constitutively activated, which causes excessive proliferation of bone.

Patient 2 has Pierre Robin Syndrome, which is a disease that results in facial abnormalities. It is inherited in an autosomal recessive fashion. This disease is caused by rearrangements or deletions on the SOX9 gene or the KCNJ2 gene. SOX9 is a transcription factor that turns on other genes involved in skeletal development and embryogenesis. A mutation in this protein is one of the reasons for abnormal ossification. Mutations upstream or downstream of SOX9 can also cause Pierre Robin Syndrome. These mutations produce proteins that are unable to interact with MSX1, a transcription factor that controls formation of structures in the mouth. This causes a fixed jaw and other oral abnormalities characteristic of Pierre Robin Syndrome.

Patient 1 has Brachydactyly type A1, which causes the middle fingers of fingers and toes to be reduced or absent. Short stature and malformed epiphyses is also common in patients with this disease. Brachydactyly type A1 is usually caused by a mutation on the BDA1B gene or on the IHH (Indian Hedgehog gene). It is inherited in an autosomal dominant fashion. While there are different types of mutations on BDA1B or IHH that can lead to the disease, missense mutations on IHH are a common pathological cause. The mutant Hedgehog protein encoded by IHH is unable to bind to a receptor called Patched-1, which is responsible for differentiation. This mutation along with others on BDA1 and IHH have the potential to prevent cellular growth, condensation and differentiation, which can lead to abnormal bone development.

A control treatment is a baseline treatment against which one or more other treatments will be compared. Depending on your question, this can be an untreated treatment, a procedural treatment, or a different treatment to that of the treatment group. Determining the appropriate control can be difficult. In an experiment done by researchers to examine how foxes and wolves affect plant communities, they set up fenced plots to exclude predators and outsiders. The hypothesis was the excluding predators in fenced plots will cause higher rodent populations, leading to greater seed predation and dispersal since rodents consume them. But, the result of this was that fenced plots had lower rodent populations because hawks would perch themselves on the fence posts and prey on the rodents. The fence posts unintentionally caused a higher predation rate inside the predator-excluded plots. A better control for this treatment would be to put posts all round the area that is being examined so that they mimic the real fence posts and all hawks don't perch solely on the posts put in for the fences.

After 14 days, 100 surviving plants were transplanted to pots and treatment fertilizer was added (Osmocote Classic 14-14-14, Scotts-Sierra Horticultural Products Company, Marysville, OH). Treatment of application of jasmonic acid and fertilizer amount was randomized, 50 plants were assigned treatment and 50 were not. The same soil used to plant the seeds was used. Half of the plants in each treatment group received one teaspoon of fertilizer, the other half received two. After application of fertilizer, plants were put onto greenhouse bench and watered. Plants were watered daily for 14 days. After 14 days, plant height was recorded on surviving plants. Non-surviving plants were discarded. Treatment of mechanical damage was done by cutting off half of some leaves and 1 spray jasmonic acid in acetone solution was applied. Control received 1 spray of acetone. Plants were placed on heat mat in greenhouse. 

Experiment begun January 19, 2019. Tomato species Lycopersicon lycopersicum, a dwarf variety to mature in 50 days, was used. Seeds used were “Tumbler Hybrid Tomato” (Lake Valley Seed, Boulder, CO). Seeds were sown into two 128-plug flats with a moist seed starter soil (Organic Starter Premium Potting Mix, Epsoma, Millville, NJ). Flats were placed on a greenhouse bench with natural light. Germination was induced by placing onto a heat mat. After 17 days in these conditions, 100 ppm N of 20-10-20 were added at every watering. The N was increased to 200 ppm after 7 days of growth.

I hypothesize that spraying jasmonic acid onto mechanically damaged plants will reduce herbivore desirability for the plants. Doing so will cause necrosis to some of the leaves of the plants which receive a normal amount of fertilizer but will not cause necrosis to the doubly fertilized plants, and the plants receiving double fertilizer will show an increased amount of defenses, such as trichomes.