zalam's blog

Professor Seydoux went onto explain what really happened in order. At the very beginning, anterior PARs stop posterior PARs from entering the membrane . When the sperm enters, it brings along a centrosome that bursts into microtubules and there was a correlation between that and the posterior PAR proteins at the membrane. Blocking of the microtubule formation of the sperm, stopped the PAR proteins from reaching the membrane. However, when the oocyte nucleus about to undergo meiotic division – the spindle formation allowed the PAR protein to access the membrane. This is suggested that it was not a question of sperm vs oocyte, it was more of a question of which cell made a rich microtubule first. In wild type, meiotic spindles are more transient, whereas the sperm asters are much more dense and stable. 

Different partitioning genes (encoding Par proteins) allowed the zygote to part into two poles. Par proteins turned out to be homologous in most eukaryotes (including humans). Loss of posterior PARs lead to expansion of anterior and vice versa. This all suggested a competition of some sort between the different PAR proteins. Kinase domains in the proteins anterior Par kinase domains phosphorylated the lipid binding domains of posterior Par proteins to stop them from accessing the membrane vice versa.

Geraldine Seydoux talked about how embryos determine body axis. She used the C.elegans as the model organism. Newly fertilized cell has two pronuclei -maternal and paternal – that fuse to one nucleus and cell division ensues to create a ball of cells. At one point the cell becomes asymmetrical – the smaller cell always ends up on the side of the posterior side and bigger cell on anterior side. But this had to be proven and linked to the adult cell. This research is shown by John Sulston who traced cell lineage of C.elegans and found that posterior side ended up being represented by the smaller cell. To dig in deeper – Professor Seydoux showed the gonads of the C.elegans (hermaphrodites) – oocytes had the maternal pronucleus and the sperms had the paternal – sperm fertilized the oocyte and the smaller cell ended up being at the posterior side, so the hypotheses were 1) the sperm determined the posterior side 2) that the oocyte directed the axis determination. They tested the first hypothesis: sperm induces posterior? They changed the position of sperm entry and the result was that that the embryo polarity was reversed. How did this work? They looked at the molecules involved in the oocyte cytoplasm. Genetic screening of wild types and mutants with symmetric cells and cloning those cells allowed them to identify the protein and their genes. 

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. 

To determine the cytoplasmic polarity, anterior side had Mex-5 protein at a higher concentration. The protein would undergo redistribution across the cytoplasm. Par-1 (posterior) phosphorylates MEX-5 and it speeds up the diffusion rate and so it is rich in the anterior side. They proved that Par-1 is necessary and sufficient by doing knockdowns of Par-1 alleles. Mex-5 had a larger complex which were more sluggish in anterior side comparison to the posterior side. The smaller complex diffused much faster from posterior on to the anterior. In terms of a model, this was described as Par-1 phosphorylating the Mex-5 to turn it into the fast species to increase the diffusion rate. 

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. 

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.

Monitoring air pollution helps to assess the quality of the air we are breathing in. The pollutants in the air can harm the respiratory system, cardiovascular system and the nervous system in humans. Furthermore, it can affect the plant and animal life all around. UMass Amherst is a model system: the inside of the campus has a burgeoning population of students and hence cars posing as a risk to the air quality, whereas the outside of the campus is richly populated with trees. This study can not only give us a sense of whether the student lives are being affected by air pollution on campus, but also helps us create a protocol that could be replicated elsewhere to assess the air quality in a simpler way.

When the sun heats up several water bodies, water vapor starts rising up due to its low density. As it reaches a higher altitude, the temperature starts to cool down. This drop results in the vapor to condense and form clouds above. A more simplified version can be shown using a cloud in a bottle. Adding a small amount of water (or to make the process much faster - ethanol) in a 1 litre plastic bottle would represent the process in a closed system. Using a rubber cork, the nozzle of an air pump can be secured in place. Once everything is set, air is pumped into the bottle with water/ethanol. As more air is pumped into the bottle, the pressure inside starts increasing. Since PV=nRT, the temperature also starts to rise inside. This equates to the water rising once the sun heats up the seas, lakes, rivers etc. As soon as the cork is removed, there is a pop sound followed by a sudden appearance of fog, which represents the cloud. When the cork is removed, there is a sudden drop in pressure, followd by the drastic drop in temperature that rapidly cools down the heated air inside, thereby causing condensation.  

The poster is very colorful but the dark color in the background is capturing too much attention away from the text. The layout is balanced appropriately. The headings are level 1 headings, but for introduction, method, discussion and neuroimaging study are not centered. The font for the body is too small. The flow of information is organized very well. It has the title, authors, a figure legend for the results and discussion. The blue background is rounded around the corners. The information is all placed in places that are easy to find. Important information was bolded. Each section is appropriately focused. There is no indentation for any of the paragraphs, but they paragraphs are indicated by leaving space in between. There are no grammatical errors and the language is appropriate. There is not an overwhelming amount of information. The  data is presented in the form of graphs with descriptive statistics (mean, standard deviation). All vectors objects are crisp and sharp.  The references are cited, giving credits to others. The poster is informative and persuasive.