jhussaini's blog

The experiment showed that melanopsin is the photopigment present on specific RGC’s that is likely to be involved in photoentrainment. Figures 1 and 2 show melanopsin positive RGC’s using immunofluorescence in rats. Melanopsin positive cells were only about 1% of the total number of RGC’s, and only a few of the melanopsin positive cells are found in the inner nuclear layer while the rest are in the ganglion cell layer. Confocal, stained images as well as digital images of melanopsin positive RGC’s were generated. The data from figures 1 and 2 showed the abundance of melanopsin on the dendrites, axons, and cell bodies in addition to the shape and structure of RGC’s. 

The authors use both mice and rats in their experiment. Mice are used because their genome is largely similar to the human genome. Rats were used because their genome is 92% similar to mice. Rats were also used because they are larger than mice, which makes them a good model organism for examining retinal circuitry. The authors first cloned melanopsin cDNA in rat cells to show that the protein sequence is nearly identical to that of mice. Then they generated specific antibodies targeting melanopsin to show the subset of cells that contained the protein. Tau-lacZ targeting shows the projections of melanopsin positive cells to the SCN and other regions of the brain. Lastly, they used a combination of immunofluorescence and Lucifer Yellow to show that intrinsically photosensitive RGC’s were melanopsin positive.

The objective for this study is to understand the mechanism of non-visual reflexes such as regulation of the circadian clock and pupillary reflexes. The suprachiasmatic nucleus (SCN) is a site for photoentrainment in the brain. A portion of light-sensitive retinal ganglion cells protrude into the SCN. The authors hypothesized that melanopsin is a photopigment on the retinal ganglion cells (RPG’s) that generate action potentials to the brain in response to light, and play a role in photoentrainment. Although it was known that some RPG’s are photosensitive, the reasons for this phenomenon were unknown. It was also known that rods and cones are not photoentraining receptors. Provided this context, the reason for the study was to understand the function of RPG photosensitivity, and to use them to study the pathway that gives rise to photoentrainment.

The publication by Abrams has a level 2 heading whereas the other one has a level 1 heading. The paper by John and Dale is structured more like a lab report following an experiment. It includes labeled figures, tables, and headings such as “abstract” and “results.” The publication by Abrams is structured more like a question-and-answer paper written in an essay format. The questions are bolded with long paragraphs that follow in response. The first paragraph of both publications gives an overview of the objective in addition to brief background information. The publication by Abrams has multiple in-text-citations in every paragraph whereas the publication by John and Dale has few in-text citations. The publication by Abrams also has many more references than that of John and Dale. This makes sense to me because the goal of the publication by John and Dale is to add new knowledge to Ecology, whereas the goal of the other paper is to present the knowledge in an understandable way. The format of each publications is tailored to its objective.

Although all of these developmental malformations impact the Hh signaling pathway in some way, they give rise to different phenotypes. These differences are visual indicators of different ways the Hh pathway can be disrupted. By discerning the gene that causes each syndrome and the molecule(s) that are disrupted as a result, you can figure out the role that the disrupted molecule normally plays in the pathway. For instance, based on the syndromes described above, you can infer that the Hh signaling pathway is responsible for eye and brain development. Knowledge of related abnormalities caused by disrupting a single pathway can elucidate the function of multiple components in the pathway and how those components interact with one another.

Malformations in the SOX9 gene can result in a variety of syndromes including Pierre Robin Syndrome, Campomelic Dysplasia, and Acampomelic Campomelic Dysplasia. In Greek, Campomelic means “bent limb,” which is a common symptom of Campomelic Dysplasia. Individuals born without bowed limbs are said to have Acampomelic Dysplasia. Both syndromes involve skeletal and reproductive malformations and are life-threatening in newborns. Malformations in the Hh signaling pathway can cause Holoprosencephaly, Microphthalamia with Coloboma, and Schizencephaly. Holoprosencephaly is an abnormality in brain development when the prosencephalon does not divide into the left and right hemispheres. Microphthalmia occurs when one or both eyeballs is abnormally small. People with Microphthalmia often have Coloboma, an anatomic abnormality in which pieces of tissue are missing from the eye. Finally, Schizencephaly is a rare birth defect that causes clefts in the cerebral hemispheres of the brain.

The paper focuses on the macroevolution of crinoids in response to sea urchin predation. Although sea urchins are more commonly known as grazers and predators that feed on coral, evidence of sea urchin bite marks on crinoids suggests a predator-prey relationship between the two. The data collected by the authors shows that bite mark frequencies increased with sea urchin diversity. It also showed that frequencies of bite marks on sessile crinoids was higher than those of motile crinoids. This result suggests that crinoids evolved to become motile as an evolutionary response against sea urchin predation during the Triassic. It also provides an explanation for why motile crinoids are more abundant than sessile crinoids in recent history. Overall, sea urchin predation on crinoids was measured by bite-mark frequencies, and the predator-prey interaction led to macroevolutionary changes in crinoids.

The main point of this paper is that sea urchin predation caused macroevolutionary changes in crinoids. Although sea urchins are more commonly known as grazers and predators that feed on coral, evidence of sea urchin bite marks on crinoids suggests a predator-prey relationship between the two. Data collected by the authors show that bite mark frequencies increased with sea urchin diversity. It also showed that frequencies of bite marks on sessile crinoids was higher than those of motile crinoids. The authors of the study hypothesize that crinoids evolved motility as a response against sea urchin predation during the Triassic. This conclusion seems plausible because motile crinoids have become more abundant than sessile crinoids in recent history. Overall, sea urchin predation on crinoids was measured by bite-mark frequencies, and the predator-prey interaction led to macroevolutionary changes in crinoids.

The design of the poster is visually appealing. Each section is enclosed by a box, making it very organized overall. The colors draw my attention but not so much that it is distracting. The headings are all blue and have the same font size and type. This adds to the organization of the poster. However, I also notice that under the some of the headings the text is bolded while the text under other headings is not. This detracts from the organization making it confusing to follow. The content of the poster is presented in a very succinct way. The bullet points make it more digestible to the readers. The figures are also clearly labeled and informative. The bold text in parts of each figure legend draw my eye to specific parts of it so I know where to look first. The tables are also nearly arranged in columns and provide a different way to represent data. Overall the poster is well constructed with only a few mishaps pertaining to design. 

Did humans or ideas evolve first? I personally think that you can’t have one without the other, and that they co-evolved in a mutualistic way. Susan Blackmore said in her Ted Talk that culture is an imitated behavior, and I believe that our genes give are responsible. But I also think many of our shared ideas and behaviors have the power to influence our genes. I think that toxic ideas can spread in a similar way to selfish genes, and that both harm individuals. The video about tide pods demonstrates that not all ideas progress to become better over time, but rather some evolve to become worse.