Post 4: Applying genetic modification and the D. radiodurans bacteria to MS

Our group is taking multiple approaches to cure multiple sclerosis including the genetic approach, interface approach, and applied cancer research approach to provide multiple paths of intervention and prevention of the symptoms and development of MS in all of its stages. Each person in our group is separately researching one of these topics in order to “fight” multiple sclerosis in different ways. I am focusing on curing multiple sclerosis on the genetic level using the Deinococcus radiodurans bacterium as a model for cell self-reparation. The D. radiodurans bacteria can withstand high amounts of radiation, destroying both its cellular components and its genome, and can fully self repair itself afterwards using extended synthesis-dependent strand annealing (ESDSA) which includes DNA polymerase I (Pol I)-dependent DNA synthesis and RecA-dependent recombination processes (Slade, 2009). These self repairing functions of the D. radiodurans bacterium is encoded in its genome specifically on chromosome II (2009). By studying what genes on the D. radiodurans’ chromosome II lead to the expression of self-reparation and using current gene editing methods such as CRISPR, it may be possible to genetically modify the human genome to promote remyelination and neuron self-reparation for cells affected by MS.

Current treatment of multiple sclerosis today includes gene therapy, modification of microglia, and t-cell therapy, all of which prove partially beneficial to treating MS but cannot fully cure it nor fully reverse the damage to cells caused by the disease. By using gene modification to edit the human genome to contain sequences that code for self-reparation of neurons and oligodendrocyte cells surrounding the peripheral and central nervous system based off of the genes on chromosome II of the D. radiodurans bacteria that code for self-reparation, full cell reparation would inhibit the progression of MS. Remyelination rates decrease as MS progresses (Podbielska, 2013). Therefore having genes that promote self-reparation would increase rates of remyelination, rebuilding the myelin sheath, and lessening the symptoms of cognitive and physical impairments associated with MS. MS could be cured without knowing the full set of genes and gene markers that cause the disease using CRISPR to edit the human genome to contain genes that promote cell reparation modeled after the ESDSA process that D. radiodurans use. Even when the immune system would cause the destruction of the myelin sheath and destruction of oligodendrocyte cells, the edited human genome would contain instructions to self-repair these cells and neurons. One gap that creates difficulties for this approach is that several of the processes that the D. radiodurans bacterium uses to repair its genome are still unknown and not fully understood. Another challenge includes that the ESDSA process of genomic reparation would need modification for application in the use of reparation for other cellular components such as the myelin sheath of the neurons. A problem that results from using CRISPR is the limited current knowledge of how using the genome of a bacteria as a model for self-repairing genes could be directly applied to editing specific genes on the human genome. Even with these challenges, gene modification to promote self-reparation of cells destroyed by MS using the D. radiodurans bacteria’s genome self-reparation as a model could lead to a direct cure of the disease and several other autoimmune diseases.

Podbielska, M., Banik, N. L., Kurowska, E., & Hogan, E. L. (2013). Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination. Brain Sciences, 3(3), 1282–1324.

Slade, D., Lindner, A. B., Paul, G., & Radman, M. (2009, March 19). Recombination and Replication in DNA Repair of Heavily Irradiated Deinococcus radiodurans. Retrieved September 28, 2018, from

Post #3: The genetic heritability and make-up of MS

In order to find a method for self repairing neurons affected by the degenerative effects of multiple sclerosis, it is necessary to understand from where multiple sclerosis originates. There is limited knowledge regarding the development of multiple sclerosis specifically in terms of genetic heritability. Family based-linkage analyses have shown MS is related to genes that encode for the human leucocyte antigen (Lin, Charlesworth, Mei, & Taylor, 2012). Furthermore genome-wide association studies have identified over 60 loci related to MS in regions of the chromosome corresponding to T-cells and the immune system (Lin, 2012). These two linkage and association studies only explain 18-24% of the heritability of MS (Lin, 2012). Many theories have been created in order to make up for the lack of knowledge about the genetic heritability of MS. The first theory includes that rare and common variants of allele frequencies related to MS that account for most of its heritability have still not been found (Lin, 2012). The second theory of epigenetics suggests that environmental factors may trigger certain gene expressions related to MS (Lin, 2012). The third theory of gene-gene interactions explains how genes of the same phenotype may have an effect on how that phenotype is expressed (Lin, 2012). The fourth theory suggests structural variants in DNA that have not been thoroughly research may hold an association between the genes and complex traits related to MS (Lin, 2012). The last theory describes how pathway involvement of congregated variants of genes may lead to susceptibility of MS and other diseases (Lin, 2012). Genetic studies still lack the methods to understand the complexity of the genes associated with MS (Lin, 2012). Without knowing the exact genes associated with MS it will be difficult to create ways to modify the cell genome in order for the myelin sheath to undergo a self-reparation process. Other ways of treating MS may need to be explored since modeling the self-reparation process of the Deinococcus radiodurans bacteria maybe difficult without knowledge of the genetic makeup of MS.

Lin, R., Charlesworth, J., Mei, I. V., & Taylor, B. V. (2012, October). The Genetics of Multiple Sclerosis. Retrieved October 11, 2018, from

Post #2: Self Reparation and Remyelination

Currently, our research of treatment of autoimmune diseases focuses on multiple sclerosis. One of the most detrimental effects of MS involves the demyelination of the myelin sheath of neurons (Podbielska, 2013). The destruction of the myelin sheath affects transmitting speed and the action potential of neurons which can severely impact mental capabilities (2013). The destruction of the myelin sheath usually results from certain proteins, paranodal and juxtaparanodal proteins, congregating on the myelin sheath and creating lesions (2013). Without the protection of the myelin sheath, the axon is vulnerable to damage from consequent electrical firing of the neurons (2013). Normally, neurons are able to repair their myelin sheath by the process of remyelination. But often the neuron’s of people who suffer from MS fail to induce this process (2013). Understanding what components of remyelination lead to the repair of the myelin sheath may offer insight into treatment for MS.

In last weeks post I researched how Deinococcus radiodurans could repair their shattered genome after undergoing extreme amounts of radiation. This week I researched more on the genome of the Deinoccocus radiodurans. Its genome comprises of chromosome I, chromosome II, a megaplasmid, and a plasmid. Chromosome II contains information regarding “amino acid utilization, cell envelope formation, and transporters” (Dassarma, 2006). Understanding how the expression of these genes leads to the full self-reparation of the Deinoccocus radiodurans bacterium and its genome could aid in understanding the generation of remyelination in neurons. Rates of remyelination decrease throughout the progression of MS (Podbielska, 2013). It involves creating new myelin sheaths over damaged demyelinated sheaths (2013). By studying the sequences of the Deinoccous radiodurans’ genome, there may be a way to genetically imitate the genes that code for self reparation in the genome of neurons.  

Podbielska, M., Banik, N. L., Kurowska, E., & Hogan, E. L. (2013). Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination. Brain Sciences, 3(3), 1282–1324.

White, O., Eisen, J. A., Heidelberg, J. F., Hickey, E. K., Peterson, J. D., Dodson, R. J., … Fraser, C. M. (1999). Genome Sequence of the Radioresistant Bacterium Deinococcus radiodurans R1. Science (New York, N.Y.), 286(5444), 1571–1577.

EN1 Website Post 1 Sofia Levy

Our group decided to research the possibility of studying Deinococcus radiodurans and their self-reparation processes in order to treat autoimmune diseases such as Multiple Sclerosis and Rheumatoid Arthritis. According to a study done in Denmark, about 9.4% of the population suffers from at least one autoimmune disease (Cooper, 2009). These autoimmune diseases occur when the immune system attacks the body itself, destroying critical tissues and organs (Bakker, 2014). While many naturalistic medicines, anti-inflammatory medications, steroids, and immunosuppressive medications may help treat and lessen the detrimental effects of autoimmune diseases, their ceases to be a way to completely cure or prevent the diseases from occurring (Bakker, 2014). Other medical procedures such as surgery or radiation treatment similarly cannot prevent or cure autoimmune diseases (Bakker, 2014). Therefore, by studying how the D. radiodurans bacterium can repair its genome after being broken into pieces by extreme amounts of radiation, there may be a way for cells affected by autoimmune diseases to fix their own DNA. Whether by replicating enzymes that catalyze the D. radiodurans’ DNA reparation and synthesis or by promoting genes that express self-reparation qualities, using the D. radiodurans as a model could help thousands of people around the world to help cure their autoimmune diseases.

While the D. radiodurans bacteria have recently become a popular topic of research, information on exactly how they self repair their genome and how to apply that information for medical benefits is still relatively unclear. What is known is that the D. radiodurans is able to withstand extreme levels of radiation, amounting up to 7 kGy (Slade, 2009). This high level of radiation breaks the genome of the bacterium about 100-150 times (Slade, 2009). In normal circumstances, most cells would not be able to recover after its DNA is shattered. But the D. radiodurans is special in that it undergoes a complex process whereby they can self-repair their genome within hours of being destroyed. About an hour and a half after the genome of the bacterium is destroyed by radiation, no DNA reparation or DNA synthesis occurs (qtd. in Slade, 2009). But within the the hour after this stagnant period, “ DNA polymerase I (Pol I)-dependent DNA synthesis and RecA-dependent recombination processes” enables the self-reparation process (Slade, 2009). It begins with extended synthesis-dependent strand annealing (ESDSA) in which strands of newly synthesized DNA are created from the original fragmented complementary strands (qtd. in Slade, 2009). These newly created strands then arrange themselves into “long linear intermediates” (Slade, 2009). Lastly, the RecA-dependent recombination process helps these fragmented pieces of DNA that were created before and after radiation enclose into circular chromosomes (Slade, 2009). By understanding the process by which the Deinococcus radiodurans utilizes DNA polymerase I (Pol I)-dependent DNA synthesis and RecA-dependent recombination processes to fix its destroyed genome, it may be possible for cells destroyed by autoimmune diseases to self-repair themselves even after being damaged by the immune system.

Bakker, E. (2014, August 26). AutoImmune Disease Causes. Retrieved September 28, 2018, from

Cooper, G. S., Bynum, M., & Somers, E. C. (2009, October 09). Recent insights in the epidemiology of autoimmune diseases: Improved prevalence estimates and understanding of clustering of diseases. Retrieved September 28, 2018, from

Slade, D., Lindner, A. B., Paul, G., & Radman, M. (2009, March 19). Recombination and Replication in DNA Repair of Heavily Irradiated Deinococcus radiodurans. Retrieved September 28, 2018, from