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fan198 fan198
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A year ago
The original strain (wild type; WT) and two mutant strains of plant X are available, mutant A (mutA) and mutant B (mutB). Dr. Mishima started Experiment 2 with all three strains growing together in a flower bed. The seeds for all three strains are “truebreeding” – in crosses among individuals of the same strain, all offspring show the same phenotype as their parents and grandparents. Dr. Mishima planted the seeds of WT, mutA, and mutB in the first five days of the experiment. The locations within the flower bed and the day of planting were randomized for the three strains but their
locations within the flower bed and strain identity were carefully noted. Fig. 2 shows the flower bed on Day 15. Fig. 3 shows when the needle-like leaves emerged in individual plants.

Q2-1 Please describe the main patterns shown in Fig. 3.

Q2-2 Dr. Mishima randomized the locations of WT, mutA, and mutB seeds within the
flower bed. Please explain why this was a part of the experimental design.

Q2-3 You would like to investigate the causes or mechanisms that coordinate the timing of emergence of the needle-like leaves among the plantlets. If you can only study one of the mutant strains, which one would you choose? Please clearly explain your choice and reasoning.

Q2-4 You can assume that mutA and mutB harbor a mutation in different proteincoding genes, genes A and B, respectively. Propose possible functions for the gene A and gene B products. Please clearly explain how your proposed functions account for the mutant characteristics observed in Fig. 3.
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Anonymous
wrote...
A year ago
a)

Needle-like leaves appeared on day-19 and -20 for the wild-type.
Needle-like leaves appeared on day-29 and -30 for mutant strain A.
Finally, needle-like leaves appeared on random days following day-19 to day-40.

b)

This was to ensure that the observations weren't influenced by nutrients being concentrated in one location and not the other. Also, some plants what the ability to communicate via chemical signals and sensory responses. By randomly choosing the planting location, this effect could be mitigated.

c)

It appears that mutant A and the wild-type are only different by a few days in their leaf emergence. Hence, if I could choose one of these, it would have to be mutant B. It is clear due to the irregular generation of leads, this strain likely has a specific genetic alteration that contribute to the observed trait difference. By comparing the mutant strain to the wild-type strain, you can pinpoint the genetic mutation responsible for the trait variation and gain insights as to what the underlying mechanism is leading to this difference.

d)

The faulty protein encoded in the mutants likely work similarly. I propose that for mutant A, the protein takes longer to mature than its wild-type counterpart. Perhaps due to a mutation, the protein has become more complex, for example having multiple domains or requiring extensive post-translational modifications cause it to take longer to mature. Once it has matured and its effects are seen (emergence of the initial leaves), a mechanism similar to the wild-type takes place, where the growth no longer takes place as we see in mutant B later on in the life cycle of the plant. Thus, the protein gets recycled or the gene responsible for the protein turns-off. The same cannot be said about mutant B since it appears like the gene responsible for the protein continues to be transcribed and translated, with no feedback loop in place to turn it off once the protein have been formed and matured.

Hope this helps! Any further questions, reply back Smiling Face with Open Mouth
fan198 Author
wrote...
A year ago
Oh, you are so smart. Can I ask you more question later, I am trying to prepare for grad school but my major is informatics right now so I dont really have people to ask.

about your c answer, I still cannot comprehend it. I thought A is better since it is only differ from wild type slightly, which probably have slight modification which we can pinpoint more accurately. Meanwhile B pattern is a bit erratic and also encompass both wild type and A duration so there might be many mutations instead which will be harder to pinpoin.

Also about your d answer it didn't really answer the function part. I just realized it is better if you read my previous question. Now I get it why c answer is mutant B, mutant B leaf emergence is not simultaneous which is why it is better to study B. I take back my paragraph before.

My assumption is similar with you for mutant A, the mutation doesn't change the simultaneous property of wild type but its duration, I assume gene A is regulating a gene that produce protein to become promoter/inhibitor of whatever that cause the simultaneous property. While I think gene B is whatever that cause the simultaneous property. so its like (gene A > gene X > gene B)

Thank you for your answer, I'd really appreciate it

Anonymous
wrote...
A year ago
Quote
Oh, you are so smart. Can I ask you more question later, I am trying to prepare for grad school but my major is informatics right now so I dont really have people to ask.

Certainly, I'll be here to help when you're ready.

Quote
about your c answer, I still cannot comprehend it. I thought A is better since it is only differ from wild type slightly, which probably have slight modification which we can pinpoint more accurately. Meanwhile B pattern is a bit erratic and also encompass both wild type and A duration so there might be many mutations instead which will be harder to pinpoin.

I picked mutant B because I figured that the genome of the wild-type and mutant A would be too similar to one another. Notice that mutant B produces the most erratic results, so the assumption is that its DNA would be most different. Also, in research, usually you would want to study the mutant over the wild-type -- I guess that also pushed my bias to using mutant B over A and the WT.

Quote
You can assume that mutA and mutB harbor a mutation in different proteincoding genes, genes A and B, respectively. Propose possible functions for the gene A and gene B products. Please clearly explain how your proposed functions account for the mutant characteristics observed in Fig. 3.

Re-reading this question, I think you're right, I did not answer it completely. We will assume Gene A produces a protein that enables emergence of leaves. Once the leaves emerge, it chemically signals the production of Gene B. Gene B stops the emergence of more leaves. In mutant A, we see this take into effect as you'd expect, with the exception that it is delayed by 1 or 2 days from the wild-type (no big deal). In mutant B, we see that the feedback effect of Gene B's protein doesn't functioning properly. When the leaves emerge as a result of Gene A, the chemical signal these leaves produce to not turn-off the protein responsible for leave emergence. In other words, the chemical that is supposed to disable Gene A's protein by activating Gene B's protein isn't working as it should. This is why we see the emergence of leaves more and more in later days. Thus, Gene B's protein is a negative feedback protein, but it is disfunctional.
fan198 Author
wrote...
A year ago Edited: A year ago, fan198
Thank you for your reply.

First, try to look at my previous question https://biology-forums.com/index.php?topic=2059458.msg5423915#msg5423915, it is the previous question before this.

Now, your assumption do make sense for me. Let me rephrase it to know if I get it correct. basically these gene A and gene B doesn't not affect each other at gene level and gene A is for start and gene B for stop, and both most likely have missense mutation that affect its effectiveness.
Anonymous
wrote...
A year ago
Yes, your understanding is consistent with my thoughts. The part about the missense mutation being the culprit is also interesting. Missense mutations, as shown in the link below are due to a single change in the amino acid sequence of the final protein. While this does not render the protein completely dysfunctional, it does cause a change in its physical structure that may lead to what we're seeing.

Looking at your linked topic, I agree with @smi3's response too. Face Screaming in Fear
Source  https://biology-forums.com/index.php?action=gallery;sa=view;id=24439
fan198 Author
wrote...
A year ago Edited: A year ago, fan198
However, now that I think it again this scenario is also possible
gene A should have 2 function: to start leaf emergence, activate gene B
gene B should also have two function: to activate gene A and communicate to other plant to do the same and to

I am assuming a certain level of protein A is needed for leaf emergence

also since the graph is per plant, and the question is not about normal leaves that each plant can have increasing number each day but needle purple leaf which each plant I assume only have one I think there is no need to stop, or the one stopping can be some other gene.

mutant A affect the leaf emergence part, but not activating gene B part. so leaf emergence should be slower, but why it happen at the same day for all plant, it is not likely normally as there must be some kind of variation. there is no variation because once 1 plant has high A it will have high B this high gene B expression is transmitted to other plant so other plant have high gene A

mutant B affect the communication part but not the activation function. that is why there is variation in time of leaf emergence, because the communication part is damaged so there is no synchronization.

this is where missense mutation come in, since it is a substitution  one part of function can be damaged while other function perfectly, that is why the mutation did not affect all functions.
Anonymous
wrote...
A year ago
Quote
gene A should have 2 function: to start leaf emergence, activate gene B
gene B should also have two function: to activate gene A and communicate to other plant to do the same and to

I agree with the first statement, but I am not following with the second. Why is gene B responsible for activating gene A? Are you implying then that Gene B must be produced first? I will look into this further tomorrow, as I didn't really consider the cross communication with other plants
fan198 Author
wrote...
A year ago
I consider multiple scenarios and gene B activating gene A is essential to get the same result as the graph. especially the mutant A graph, in which the gene B is not damaged. it is not activating but more like gene A and gene B is positive feedback looping each other. I think gene B main function is to keep gene A expression high in all plants.

No, gene A is okay without gene B, but gene B is harmonizing the level of gene A across all plants.

since they are okay without each other it means that they are not binding at promoter region but at enhancer region I think. if a gene need another gene it means that the promoter region is the one that is affected.
Anonymous
wrote...
A year ago
since they are okay without each other it means that they are not binding at promoter region but at enhancer region I think. if a gene need another gene it means that the promoter region is the one that is affected.

I don't think this part is not necessary in our explanation. In fact, with the information provided, it is impossible to make this assumption without further evidence. Both genes can have their own 5' upstream region and it would not impact the results.
fan198 Author
wrote...
A year ago
Yes, I agree assuming that much detail is too much. I will post another question later. The last question is how you would design a research from this info, with methodology etc, which I think is too broad to be asked as a question
Anonymous
wrote...
A year ago
I thought the question did a good job already describing the methodology? Grinning Face with Smiling Eyes

Probably the method for testing our hypothesis about the linked gene hypothesis we came up with... right? If so, I wouldn't be hard to write.
fan198 Author
wrote...
A year ago
Yes, I think it is easier that way since the way the question structured is leading you toward that particular way. It just that, we can freely choose the data such as genome, transcriptome, proteome in addition to this experiment, and said that you can choose any topic related to the question above which makes it a bit broader. I just think it is better to stray a bit from that to idk demonstrate creativity or something like that. I am thinking about the protein structure since I assume the mutant change only a bit to hinder some function. If I used mRNA level the mutant and the wt surely will be expressed at similiar level since olny the coding region is affected.
Anonymous
wrote...
A year ago
You've shared a brilliant line of questions (this topic and the other you started) actually. These are smart biology questions, ones that I haven't seen in many years answering questions that get asked on this forum. That being said, based on the information provided in your other question (the one about intestinal stem cell overproliferation), I can see why you opened the door to discussing promoter/enhancer regions when it wasn't directly suggested.

It's important to note that there can be many theoretical explanations, and which ever avenue you take, in reality, it would require extensive experimental validation to confirm whether it is true or not. I don't think the instructor will mind if one hypothesis is more wild than the next, but simplicity is equally important. Remember that extraordinary claims require extraordinary evidence!
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