Skip to main content

Small Non-coding RNA in Your Food!: PSTVd

Figure 1. Tomato plant infected with PSTVd.

Have you ever encountered a funny looking plant that makes you think, “I shouldn’t eat this” by instinct? Maybe it was an OK crop that just looks weird, but it is possible for plants to catch ‘diseases’ as well, just like humans. Viruses can infect many hosts, from humans to small microorganisms. These viruses take advantage of living organisms, using the host to replicate themselves and eventually end up ‘killing’ the host if left unattended.


Figure 2. Comparison of potatoes with or without PSTVd.

PSTVd is one of these viruses that makes most of plants (aka your food) sick. PSTVd is short for Potato Spindle Tuber Viroid; it obtained that name by being found in potatoes for the first time. Symptoms of viroid infection in plants include stunting of growth, deformation of leaves and fruit, stem necrosis, and death. In the case of PSTVd affected potato, the plants show stunting of the plant and malformation and cracking of tubers. Although it is named after potato specifically, it is able to infect many different types of hosts. PSTVd is known for being the first identified viroid.



Figure 3. Secondary structure of PSTVd.



Viroids are the smallest infectious pathogens known. They are single stranded RNA without protective protein coating. A viroid is known to infect plants only (with a few exceptions). Some, such as PSTVds, causes harmful diseases while others can be benign. While viruses can be considered parasites of host translation machinery, viroids are parasites of cellular transcription proteins.

Figure 4. Size comparisons of viruses to human blood cell.

It is amazing how such a small RNA can have a great impact on an entire organism, like a plant. Viroids are extremely small. They have an average width of 2nm and length of 40 -130nm. Think about how small that actually is. They are even smaller than virus, which is considered much smaller compared to cells. So you may be wondering how such a small structure can destroy a much bigger host. This small RNA, PSTVd, can replicate itself in hosts and makes potatoes (and other crops) sick.

What’s the mechanism of how this RNA causes diseases in hosts? Great question. We don’t really know. Here are the observations of what we know:
  1. Viroids need cellular RNA polymerase to replicate
  2. This polymerase, which normally transcribes DNA templates copies viroid RNAs
  3. RNA splicing, a process that removes the non-coding sequences from pre-mRNA and joins the protein-coding sequences together, might be a key player in how PSTVd causes diseases in plants 
And here is a list of few of the countless things that we not yet understand:
  1. The exact mechanism of how viroid infections lead to severe symptoms in plant hosts
  2. Which biological pathways in the plant infection by PSTVd affects
  3. What determines mild/benign symptoms to severe symptoms
To understand these unknowns, scientists are looking into the mechanism of viroid replication. Here’s what they’ve learned:

In plants that are infected with viroids such as PSTVd, viroid RNA is imported to the nucleus and gets copied by plant RNA polymerase II. The copied viroid produces complementary linear RNAs. These RNAs are copied again to produce linear molecules, which are cleaved by the host enzyme Ribonuclease III. Ribonuclease is an enzyme that catalyses breakdown and processing of RNAs. When the linear viroid RNAs are cleaved, their ends are joined by a host enzyme to form circular forms.


Figure 5. Viroid RNA entering nucleus.

After replication, viroid progeny exit the nucleus (or chloroplast) to move to adjacent cells through plasmodesmata (systemical travel via the phloem) to infect other cells. Viroids enter the pollen and ovule, from where they are transmitted to the seed. When the seed germinates, the new plant becomes infected.

Scientists were able to discover the replication mechanism of many viroids including PSTVd, but there is so much still to learn about how this tiny non-coding RNA can make potatoes or tomatoes sick. Maybe you, as a future researcher, can discover more about the other viroids and how such a small RNA affect biological pathways in hosts to deliver severe symptoms.

References
1. Adkar-Purushothama, C. R., Iyer, P. S., & Perreault, J. (2017, August 21). Potato spindle tuber viroid infection triggers degradation of chloride channel protein CLC-b-like and Ribosomal protein S3a-like mRNAs in tomato plants.

2. Dillon, Mukkara, P., Owens, R. A., Baumstark, T., & Bruist, M. F. (2017, December 15). Processing of Potato Spindle Tuber Viroid RNAs in Yeast, a Nonconventional Host.



3. López-Carrasco, A., Ballesteros, C., Sentandreu, V., Delgado, S., Gago-Zachert, S., Flores, R., & Sanjuán, R. (2017). Different rates of spontaneous mutation of chloroplastic and nuclear viroids as determined by high-fidelity ultra-deep sequencing. PLOS Pathogens, 13(9). doi:10.1371/journal.ppat.1006547

Comments

Popular posts from this blog

Transposons in reverse: a blessing or a curse?

Summary of main points Retrotransposons are a type of mobile genetic element (MGE) that can copy and paste themselves multiple times throughout the genome using an RNA intermediate. Retrotransposons are widely considered to be harmful and bad for cells. They resemble retroviruses and our cells have developed mechanisms to protect against retrotransposition.  The prevalence of retrotransposons throughout the tree of life suggests they are evolutionary important. This contrasts the negative effects that can cause in cells.  Retrotransposons are suggested to generate more genetic diversity locally and globally in a genome, which is consistent with their prevalence in humans among other species. The glossary at the end of the post may have some helpful information should you need it :)  Figure 1: The mechanism of DNA transposition. In the past ten years alone, the study of mobile genetic elements (MGEs), or DNA sequences that can move around within a genome or between s

The RNase (P) for everyone

Ribonuclease P, or RNase P for short, is a catalytic RNA found in nearly every organism on earth (Fig 1). Discovered in 1978 by Stark, Kole, Bowman, and Altman, RNase P was the second type of ribozyme, an RNA that does the work of a protein, discovered, and the first to act exclusively on sequences not part of the same molecule as itself (1). While it was initially thought that both the RNA (called P RNA) and associated protein were necessary, further studies showed that the RNA alone has catalytic activity, making huge waves in the enzyme world (2). Figure 1 . RNAase P RNA structure across all domains of life and hypothesized "RNA world" with associated proteins. Adapted from Walker et al. 2008 P RNA folds into multiple helices and loops (Fig 2A) that connect with each other through base pairing (A-U and C-G) like in DNA and base stacking where the rings in each base stack and stick on top of each other to form a very stable structure (Fig 2B). Across all domains of

IRES: The Trojan horse of Hepatitis C

Ana was 22 years old when she found out she had it… Hepatitis C! Unlike others her age, she hadn’t yet had a boyfriend, gotten tattoos in non sterile conditions, damaged her liver by excessive drinking in college, or shared needles to inject drugs, all of which are ways one can get the disease (1). All she had done was receive a kidney (a solid organ) from her uncle who was born in 1962 in Japan, one of the few industrialized countries with high Hepatitis C rates (2). She first noticed the massive bruises on her arms and legs 6 months ago followed by the yellowing of her eyes (jaundice). Her doctor thought it was her body rejecting the kidney and causing her to have reduced platelets but after getting a biopsy, it turned out her liver had become cirrhotic and was failing. Cirrhosis is a chronic disease that leads to inflammation which, over time, replaces healthy liver cells with scar tissue. It takes about 20 to 30 years for this to happen (or faster if alcohol is drunk or if someon