Peer Review History
| Original SubmissionNovember 16, 2021 |
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Dear Dr. Yan, Thank you very much for submitting your revised manuscript "Turnip mosaic virus co-opts the vacuolar sorting receptor VSR4 to promote viral genome replication in plants by targeting viral replication vesicles to the endosome" for consideration at PLOS Pathogens. As with all papers reviewed by the journal, your manuscript was reviewed by members of the editorial board and by several independent reviewers. The reviewers appreciated the attention to an important topic. Based on the reviews, we are likely to accept this manuscript for publication, providing that you modify the manuscript according to the review recommendations. Please prepare and submit your revised manuscript within 30 days. If you anticipate any delay, please let us know the expected resubmission date by replying to this email. When you are ready to resubmit, please upload the following: [1] A letter containing a detailed list of your responses to all review comments, and a description of the changes you have made in the manuscript. Please note while forming your response, if your article is accepted, you may have the opportunity to make the peer review history publicly available. The record will include editor decision letters (with reviews) and your responses to reviewer comments. If eligible, we will contact you to opt in or out [2] Two versions of the revised manuscript: one with either highlights or tracked changes denoting where the text has been changed; the other a clean version (uploaded as the manuscript file). Important additional instructions are given below your reviewer comments. Thank you again for your submission to our journal. We hope that our editorial process has been constructive so far, and we welcome your feedback at any time. Please don't hesitate to contact us if you have any questions or comments. Sincerely, Savithramma P. Dinesh-Kumar Associate Editor PLOS Pathogens Peter Nagy Section Editor PLOS Pathogens Kasturi Haldar Editor-in-Chief PLOS Pathogens orcid.org/0000-0001-5065-158X Michael Malim Editor-in-Chief PLOS Pathogens *********************** Reviewer Comments (if any, and for reference): Reviewer's Responses to Questions Part I - Summary Please use this section to discuss strengths/weaknesses of study, novelty/significance, general execution and scholarship. Reviewer #1: This manuscript addresses the identification of AtVSR4 as an interactor of TuMV 6K2 protein and aims to characterize its role in targeting 6K2 to the enlarged late endosome for efficient viral infection instead of using the conventional VSR-mediated pathway from early to late endosome. The authors report VSR4 mutants defective in trafficking and non-N-glycosylated forms that support stronger viral replication than the wild type VSR4. At the same time, the virus promotes VSR4 accumulation and hijack glycosylated VSR4 for its protection from autophagy pathway. The manuscript is original and provides a large amount of information on the role of 6K2 co-opting VSR4 and the way they are able to traffic to promote viral replication. These results are relevant for the plant-virus community. The methodology is adequate. The manuscript is dense to read probably because it has a large amount of information. Overall, it is well written. The doubts I had referred to mutants and non-N-glycosylated VSR4 promoting viral infection. Then, wild type VSR4 would be somehow down controlling viral infection. However, this question has already been addressed by the authors in response to the previous reviewers and included in the new version. Thus, I have no further requirements. Reviewer #2: This manuscript continues recent investigations on ER-derived 6K2-induced vesicles and how they utilize an unconventional Golgi-bypassing pathway and enlarged late endosomes to induce a productive turnip mosaic virus infection. The authors show through extensive experimental work that vacuolar sorting receptor 4 (VSR4) has a specific role in this process through its interaction with the 6K2 protein. The authors demonstrate that QYMDS sequence at a C-terminal domain of VSR4 serves as a binding site and when this sequence was substituted with five alanine residues both 6K2 binding and CP accumulation were reduced (Fig. S3). All conditions that increased the amount of VSR4 and those mutations in it which prevented its normal function in Golgi traffic, enhanced 1) the amount of unconventional bypass of 6K2-vesicles from cis-Golgi to enlarged late endosomes and 2) both (+)- and (-)-strand TuMV RNA accumulation. N-glycosylation is used for the turnover regulation of VSR4. TuMV infection increased the amount of VSR4 on protein but not on mRNA level, which proposes that TuMV can affect the degradation of glycosylated VSR. The authors have done a substantial revision and added a lot of data to this revised version. I find the presented data very interesting. ********** Part II – Major Issues: Key Experiments Required for Acceptance Please use this section to detail the key new experiments or modifications of existing experiments that should be absolutely required to validate study conclusions. Generally, there should be no more than 3 such required experiments or major modifications for a "Major Revision" recommendation. If more than 3 experiments are necessary to validate the study conclusions, then you are encouraged to recommend "Reject". Reviewer #1: (No Response) Reviewer #2: Among the added data is Fig S3 in which it is shown that QYMDS to AAAAA substitution in C-terminus of VSR inhibited the VSR4 binding to 6K2 and reduced TuMV CP accumulation. The quantitation of CP accumulation is missing from this figure. In the case of other VSR4 mutants as well as when over expressed or down regulated, the authors demonstrate viral RNA accumulation. How does OE of VSR-C1A mutant alter the (+)- and (-)-strand synthesis? I don’t agree yet with the statement that VSR4-6K2 interaction is critical for TuMV infection. ********** Part III – Minor Issues: Editorial and Data Presentation Modifications Please use this section for editorial suggestions as well as relatively minor modifications of existing data that would enhance clarity. Reviewer #1: (No Response) Reviewer #2: Chloroplast fluorescence is hardly visible in Fig 3C 48h. It is difficult to detect the signal also in 3E Col FM4-64 and avr4 mutant mCherry ARA Q69I panels. ********** PLOS authors have the option to publish the peer review history of their article (what does this mean?). If published, this will include your full peer review and any attached files. 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Data must be deposited in an appropriate repository, included within the body of the manuscript, or uploaded as supporting information. This includes all numerical values that were used to generate graphs, histograms etc.. For an example see here: http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001908#s5. Reproducibility: To enhance the reproducibility of your results, we recommend that you deposit your laboratory protocols in protocols.io, where a protocol can be assigned its own identifier (DOI) such that it can be cited independently in the future. Additionally, PLOS ONE offers an option to publish peer-reviewed clinical study protocols. Read more information on sharing protocols at https://plos.org/protocols?utm_medium=editorial-email&utm_source=authorletters&utm_campaign=protocols References: Please review your reference list to ensure that it is complete and correct. If you have cited papers that have been retracted, please include the rationale for doing so in the manuscript text, or remove these references and replace them with relevant current references. Any changes to the reference list should be mentioned in the rebuttal letter that accompanies your revised manuscript. If you need to cite a retracted article, indicate the article’s retracted status in the References list and also include a citation and full reference for the retraction notice.
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| Revision 1 |
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Dear Dr. Yan, We are pleased to inform you that your manuscript 'Turnip mosaic virus co-opts the vacuolar sorting receptor VSR4 to promote viral genome replication in plants by targeting viral replication vesicles to the endosome' has been provisionally accepted for publication in PLOS Pathogens. Before your manuscript can be formally accepted you will need to complete some formatting changes, which you will receive in a follow up email. A member of our team will be in touch with a set of requests. Please note that your manuscript will not be scheduled for publication until you have made the required changes, so a swift response is appreciated. IMPORTANT: The editorial review process is now complete. PLOS will only permit corrections to spelling, formatting or significant scientific errors from this point onwards. Requests for major changes, or any which affect the scientific understanding of your work, will cause delays to the publication date of your manuscript. Should you, your institution's press office or the journal office choose to press release your paper, you will automatically be opted out of early publication. We ask that you notify us now if you or your institution is planning to press release the article. All press must be co-ordinated with PLOS. Thank you again for supporting Open Access publishing; we are looking forward to publishing your work in PLOS Pathogens. Best regards, Savithramma P. Dinesh-Kumar Associate Editor PLOS Pathogens Peter Nagy Section Editor PLOS Pathogens Kasturi Haldar Editor-in-Chief PLOS Pathogens orcid.org/0000-0001-5065-158X Michael Malim Editor-in-Chief PLOS Pathogens *********************************************************** Reviewer Comments (if any, and for reference): |
| Formally Accepted |
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Dear Dr. Yan, We are delighted to inform you that your manuscript, "Turnip mosaic virus co-opts the vacuolar sorting receptor VSR4 to promote viral genome replication in plants by targeting viral replication vesicles to the endosome," has been formally accepted for publication in PLOS Pathogens. We have now passed your article onto the PLOS Production Department who will complete the rest of the pre-publication process. All authors will receive a confirmation email upon publication. The corresponding author will soon be receiving a typeset proof for review, to ensure errors have not been introduced during production. Please review the PDF proof of your manuscript carefully, as this is the last chance to correct any scientific or type-setting errors. Please note that major changes, or those which affect the scientific understanding of the work, will likely cause delays to the publication date of your manuscript. Note: Proofs for Front Matter articles (Pearls, Reviews, Opinions, etc...) are generated on a different schedule and may not be made available as quickly. Soon after your final files are uploaded, the early version of your manuscript, if you opted to have an early version of your article, will be published online. The date of the early version will be your article's publication date. The final article will be published to the same URL, and all versions of the paper will be accessible to readers. Thank you again for supporting open-access publishing; we are looking forward to publishing your work in PLOS Pathogens. Best regards, Kasturi Haldar Editor-in-Chief PLOS Pathogens orcid.org/0000-0001-5065-158X Michael Malim Editor-in-Chief PLOS Pathogens |
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