Bacterial Conjugation

As we learned in class, gene transfer in bacteria can occur through transformation, transduction, and conjugation. In this post, I will be focusing on conjugation. In conjugation, there is direct contact between the donor cell and the recipient cell through which a strand of DNA is transferred. See the picture below for a visual of how conjugation occurs. It has been found that conjugative plasmids contain genes that are resistant to several types of antibiotics. Therefore, if resistance to a particular antibiotic is selected, resistance to other types of antibiotics will be simultaneously selected. Plasmids involved in gene transfer also code for conjugative pilli that facilitates the transfer of DNA by binding to the recipient cell from the donor cell. At the end of conjugation, both cells have the plasmid that was transferred.



According to my article, this is the main method of the transfer of antibiotic resistance between bacteria. It may be useful to develop a method of preventing conjugation in order to prevent the development of bacteria that are resistant to multiple antibiotics. Several decades ago, it was found that filamentous bacteriophages are capable of preventing conjugation. Further investigation showed that this was accomplished by closing up the conjugation pilus (or sex pilus). This is mainly mediated by g3p, a phage protein within the phage coat that seems to lower conjugation rates. These results indicate that certain proteins from the phage can be used to slow down antibiotic resistance in bacterial cells.

Click here to view the abstract of the article I used and click here to view the full article.

To Share and Share Alike

This chapter in biology has been all about the genetics of viruses and bacteria. One of the topics that we covered in class was horizontal gene transfer, in which genetic information is trasnferred between bacterial cells. This leads to increased genetic variation. I found the picture below to be helpful in understanding the difference between horizontal and vertical gene transfer.

According to my article, it was originally thought that horizontal gene transfer in bacterial cells only occurred in certain situations, such as in the presence of strong antibiotics. In actuality, prokaryotes (which include bacteria and archaea) are able to receive genes rather frequently either through a bridge or a virus. This can even occur when the two prokaryotes transferring genes are from different species. Researchers have found that 88 to 98% percent of new genes in bacteria come from horizontal gene transfer. The genes that are transferred are usually next to genes that are not similar in function. Genes that evolve within a bacteria are often located near genes that serve similar functions. The study shows that the majority of new DNA in bacteria comes from horizontal gene transfer. It has also been observed that newly transferred DNA usually stay longer within the genome and evolve more efficiently. Overall, horizontal gene transfer allows prokaryotes to evolve quickly to fit a new environment. This is also the cause of rapid development of antibiotic resistance in bacteria.

To access the article from which I retrieved my information, click here.

Dihybrid Crosses Video

Embarrassing as it might be to admit, I forgot how to do dihybrid crosses between freshmen year and now. I did not find the book to be particularly helpful in explaining this, so I found this video:

He uses traits in mice, the grasshopper phenotype and the prune phenotype, to set up a cross. I particularly liked how he explained what happened if the genes were linked (on the same chromosome) and if they were independently assorted. I also liked how he used the pictures of chromosomes to really explain how these crosses occur, very similar to what Dr. Weber did in class. Later on in the video, he goes through what happens when two genes are linked, using a CSP (craniofacial and skeletal malfunction) phenotype that is on the same chromosome as the grasshopper phenotype. He uses the appropriate terminology throughout the video and I appreciated his use of the terms "parental" and "recombinant". Sometimes, Youtube video makers are rather incompetent when it comes to terminology, but thankfully he is not! He also briefly touches on the probability aspects of dihybrid crosses. I also learned something new when at the end of the video he talked about map units and what they measure. The last think I liked about his explanation was how he explained the proper way to write the genotype of the mouse, with regards to the linkages of the genes.

Diseases for Darwinism

This article discusses Huntington's disease, what causes it, and the other effects that having this disease can have besides the classic symptoms. Huntington's disease is a neurological disorder that destroys neurons in certain regions of the brain. This causes the patient to have difficulty controlling movements. This can lead to various cognitive and emotional problem. This disease occurs due to a mutation that leads to the abnormal elongation of a gene known as huntingtin. The length of this gene becomes problematic when it exceeds past a certain extent and the length has an impact on the severity of symptoms.

Animals with this type of mutation only develop Huntington's when they make p53 (the tumor suppressor we learned about in Chapter 14!). Studies at Tufts University have found that people with Huntington's disease are less likely to have cancer and have more children than the average person. It is possible that increased p53 plays a role in these "side effects" of Huntington's. This is because, as we have previously learned, p53 regulates cell division and helps prevent cancers. The article goes on to talk a little bit more about p53 and its link to Huntington's. However, I want to get more into the material that is related to Chapter 16. As we know, Chapter 16 is about simple patterns of inheritance. As we have also learned in class, Huntington's disease is autosomal dominant. Look at this nifty picture to see how this disease is passed down generations:

The mutated gene is located on an autosomal (non-sex) chromosome and a person needs only one copy of the mutated gene for them to express the disease. As you can see in the picture above, the father is heterozygous for Huntington's but expresses the disease since it is dominant. Because he has children with a normal woman, 50% of his kids are unaffected while the other 50% are affected. I retrieved this infromation from here. If you are curious about Huntington's this site is extremely reliable and has a brief overview of the disease as well as detailed explanations.

The information in the previous paragraph is mostly review (since we have discussed the autosomal dominant nature of Huntington's in class), and I would also like to discuss another aspect of the Scientific American article that relates to our current chapter. A biologist at Tufts, Philip Starks, who has been studying p53 and Huntington's (as mentioned before) suspects that Huntington's is an example of antagonistic pleiotropy. Pleiotropy is when a mutation in a single gene results in multiple effects on the individual's phenotype. There are several forms of pleiotropy. One is when a single gene expression can alter cell function in more than one way. Another is when different cell types express a gene within a multicellular organism. Finally, one gene may be expressed at different phases of development. Check out pg. 343 in our biology textbook for even more information regarding pleiotropy. Starks believes that Huntington's may be pleiotropic because the same protein that results in the debilitating symptoms of Huntington's may also be responsible for making Huntington's patients more reproductively successful.

Gene Therapy and X-Linked SCID

In class this week, we learned about various patterns of inheritance. These included simple Mendelian inhertiance, incomplete dominance, codominace, sex-influenced inheritance, and X-linked inheritance. For this blog post, I am focusing on the last of these types of inheritance patterns.

X-linked severe combined immunodeficiency, or SCID, is a disease that causes people to not have functioning immune systems, leaving them susceptible to life-threatening infections. This disease results from a lack of T cells and natural killer cells as well as nonfunctional B lymhocytes (remember these from A&P?). Children with this disease are usually diagnosed to the recurrence of infections despite normal treatment. The final diagnosis of X-SCID is done by checking lymphocyte counts, lymphocyte functionality tests, and testing of the molecular genes. The best treatment for SCID is a bone marrow transplant from a genetically matched sibling. In the absence of such a sibling, unmatched donors are often recruited to donate bone marrow although these transplants are only about 70 percent successful.

As seen in the name of the disease, the inheritance of this condition is X-linked. This condition is more likely to occur in males, since they only have one X chromosome. Therefore, there is no recessive or dominant involved in their inheritance. In a female, it is possible to have recessive X-linked conditions that are not expressed due to the presence of normal genes on the other X chromosome. This is not an option for males, since they have an X chromosome and a Y chromosome. If a mother is a carrier for this disease, the chance of her transmitting this gene is 50%. Males who have SCID can only pass this gene on to their daughters, and not their sons. As we know from what we learned in class, this is because an X chromosome is contributed to daughters while a Y chromosome is contributed to sons. It is possibly for prenatal testing to be conducted on women to determine if they are carriers for this disease.

Feel free to read this article, from which I retrieved my information, to understand more about this disease. I mainly attempted to focus on the information that was relevant to our current chapter of patterns of inheritance.

Meiosis Video

I found this video useful because ever since freshmen year, I have had difficulty differentiating what to call "chromosomes", "sister chromatids", and "homologous chromosomes". Even Ms. Patil couldn't understand why I couldn't understand meiosis properly! And when Dr. Weber explained it, I understood it for about 5 minutes before once again I was confused. In a way, watching this brief video on meiosis helped me figure out these terms. While it does not go in depth, the video hits all the major points of meiosis. It goes from interphase through the second cytokinesis. It even mentions crossing over and how it occurs. My only complaint is that it does not mention how errors might occur during meiosis. Of course, one can always refer to my previous blog post for that!

As a quick addition, I would like you to view this image:

Typical Sexual Cycle for Humans	Typical Sexual Cycle for Protists
and Other Animals

Diploid Phase       Haploid Phase


that I retrieved from here. While its just a simple image, it clarified my confusion over what diploid-dominant and haploid-dominant species were. For some reason, the description in the book was somewhat confusing to me. Here, the image on the left displays the cell cycle of a diploid-dominant species while the image on the right displays the cell cycle of a haploi-dominant species.

Surprises in Cell Division

As promised, this summary as well as this article are shorter than those of my previous post. So, without further ado...

A research group at the California Institute of Technology has been able to capture the first three-dimensional image of cell whose nucleus is dividing in high resolution. A new method of cell slicing and imaging were used that allowed for the image to be obtained. While conventional electron microscopy involves much handling of the specimen prior to viewing, a technique called electron cryptomography, or ECT, was used trap the specimen in a more native manner, encasing it in a thin layer of ice. A limitation is that ECTs require the sample to be 500 nanometers thick at the most. The smallest known eukaryote was used and even that needed to be sliced carefully using a machine and a diamond knife.

Now that we know why what the researchers at CalTech did allowed them to capture the image while others previously could not, let's move on to the cell division aspect of this. I will refrain from going in depth regarding how mitosis works, as we discussed this quite thoroughly in class. During metaphase, the sister chromatids line up at the center of the nucleus, where they are held by microtubules in the form of a mitotic spindle. In most fungi, plants, and animals, more than one microtubule attach to each chromosome prior to the separation of the chromosome sets. In the image taken by the researchers at CalTech, a cell with 20 chromosomes is present, but only 10, somewhat incomplete microtubules were found. I was quite surprised when I read this because in all the pictures in our bio books and the pictures we drew in class, there was at least one kinetechore microtubule per sister chromatid set.
This is sort of how I have always pictured mitotic metaphase:

Note that I pictured it with one microtubule per sister chromatids

This leads to the question of how the sister chromatids separated. The researchers hypothesized that perhaps the chromosomes bundled up so that they could be separated by a fewer number of microtubules. Further studies using this slicing and imaging technique might lead to new discoveries in several kinds of cells, including human cells.

The top image shows multiple microtubules per set while the bottom picture show the bundling of chromosomes idea that fits with the information found in the study

Click here to view the article.