Talk:WikiJournal of Science/Grainyhead-like Genes in Regulating Development and Genetic Defects

Latest comment: 5 years ago by Evolution and evolvability in topic Review 2

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<meta name='citation_doi' value='10.15347/wjs/2020.002'>

Article information

Authors: Tyler Rushton[a]  , Sebastian Dworkin[a][i]  

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  1. 1.0 1.1 La Trobe University, Department of Physiology, Anatomy and Microbiology.
  1. s.dworkin@latrobe.edu.au

 

 

 Comparison of WT (a, c) and Grhl3 KO (b, d) mice embryos at 18.5 days poss fertilization. It shows that Grhl3 KO mice have a shortened and flattened skull that is smaller in size overall, with a lack of vascularisation at the sutures. a-b are shown from a lateral view while c-d are shown from a dorsal view.[1]


Stephen Goldie, et al, CC BY

Plagiarism check


Review 1


Review by anonymous peer reviewer ,
These assessment comments were submitted on , and refer to this previous version of the article

The article gives a comprehensive overview of the various functions of Grainyhead genes and the defects that arise in Grh mutant organisms.

There are some references that could be altered for accuracy. Also, while most phenotypes have been described in mice, causal mutations have been described in humans and additional phenotypes in fish – specifiying which model is referred to would make the review more clear.


Grhl2

I’d suggest a re-ordering of the list of descriptions of phenotypes of Grhl2 mutant mice, I would suggest that ‘split face’ and neural tube defect phenotypes are the most striking. In mice the smaller lower jaw is less immediately notable - partly because of the early lethality.

In the line ‘there was incomplete closure of these structures, leading to spina bifida and thoracoabdominoschisis following loss of Grhl2 function (Pyrgaki et al., 2011)[18]’ it would be more accurate to cite Werth 2010 , Rifat 2010 and/or Brouns 2011. The mouse described by Pyrgaki et al exhibits exencephaly but not spinal bifida – all these references could be included for the ‘split face’ phenotype.

The review does not refer to the fact that over-expression of Grhl2 also causes spina bifida (Brouns 2011)


Grhl3

Similarly, for Grhl3 the primary defect – most obvious in all the mouse models is neural tube defects and skin barrier defects. So I would suggest that

‘Primarily, Grhl3 seems vital for the development of the craniofacial skeleton (Goldie et al., 2016)[1]’ could be shifted to after these defects or refine the description to state ‘In humans, Grhl3 plays a key role in development of the craniofacial skeleton’.

It is not correct to state that ‘Grhl3 is also expressed in the brain of mice embryos, unlike Grhl1 and Grhl2’. Grhl2 is expressed in the embryonic brain – is the author referring to fetal or post-natal stages?

Over-expression of Grhl3 has also been shown to cause spina bifida (De Castro 2018)


Table

As might be expected the authors have reference primarily their own groups work in the table. For completeness I would suggest inclusion of: Werth 2010, Pyrgaki 2011. Brouns 2011 – grhl2 – exencephaly, split face, spina bifida,

Gustavsson 2007, Yu et al 2006 - Grhl3 – spina bifida. It is also unclear why Carter 1969 is referenced here?

The references for spina bifida over-expressing grhl2 and Grhl3 (see above) are also missing from the table. It would be worthwhile to point out these findings as it emphasises the crucial requirement for regulation of Grhl gene expression levels.

Skin barrier defects (Ting 2005), and post-natal wound healing (Gordon 2014) should also be included in the table.

Response

Peer reviewer, Your feedback was greatly appreciated and the issues raised in your review were extremely constructive. The references within the article were changed, added and/or removed based largely on your recommendations, with others also added to follow in aiding the article's strength. The structure of some of the paragraphs were also altered to help give the article a more coherent structure and to help lead the reader through content. Overall, all feedback was taken on.

Review 2


Review by Ulla Hansen (with Sarah Yunes, graduate student) , Boston University
These assessment comments were submitted on , and refer to this previous version of the article

This article is concise and yet covers rather extensively and accurately the findings regarding the Grainyhead-like gene family as it relates to development and disease. It therefore is a useful overview of this area, although it only peripherally explores the molecular mechanisms underlying the regulation of epithelial cell behavior in development.

However, some of the language is unclear or convoluted, and therefore edits in the body of the text.were proposed to clarify the meaning. In addition, comments were added to indicate instances in which the authors need to revise the text, as the intended meaning was not always obvious, and the language occasionally made confusing what is cause and what is effect.

Changing the title is also recommended, as it does not accurately represent the scope of the article; in particular, the biochemical and molecular mechanistic aspects of this protein family are not discussed in any detail. The title should be modified to reflect the focus on the role this gene family in regulating development (as well as the disease consequences of mutations in these genes).

Overall, with relatively minor edits, this review is solid and useful, and a worthy addition for the WikiJournal of Science.

Response

Dear Ulla and Sarah, thank you for your feedback. As per your feedback, the article has been modified to help have it read clearer and in a more structured manner. The title change recommendation was an excellent idea and was implemented so that the title now reflected better what the article is covering more specifically. Overall, I want to thank you for your time and for your contributions to this article

Summary of changes by authors in response to peer reviewer comments at this link.
T.Shafee(Evo﹠Evo)talk 09:28, 17 December 2019 (UTC)Reply

  1. Goldie, Stephen J.; Arhatari, Benedicta D.; Anderson, Peter; Auden, Alana; Partridge, Darren D.; Jane, Stephen M.; Dworkin, Sebastian (2016-10-18). "Mice lacking the conserved transcription factor Grainyhead-like 3 (Grhl3) display increased apposition of the frontal and parietal bones during embryonic development". BMC Developmental Biology 16 (1). doi:10.1186/s12861-016-0136-7. ISSN 1471-213X. PMID 27756203. PMC PMC5070091. http://bmcdevbiol.biomedcentral.com/articles/10.1186/s12861-016-0136-7. 
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