@article{Morata_1977,
  doi = {10.1016/0012-1606(77)90266-4},
  url = {https://doi.org/10.1016%2F0012-1606%2877%2990266-4},
  year = {1977},
  month = {apr},
  publisher = {Elsevier {BV}},
  volume = {56},
  number = {2},
  pages = {227--240},
  author = {Gines Morata and Peter A. Lawrence},
  title = {{The development of wingless a homeotic mutation of Drosophila}},
  journal = {Developmental Biology},
}


@article{Yang3695,
  author = {Yang, X. and van Beest, M. and Clevers, H. and Jones, T. and Hursh, D.A. and Mortin, M.A.},
  title = {{decapentaplegic is a direct target of dTcf repression in the Drosophila visceral mesoderm}},
  volume = {127},
  number = {17},
  pages = {3695--3702},
  year = {2000},
  publisher = {The Company of Biologists Ltd},
  abstract = {Drosophila T cell factor (dTcf) mediates transcriptional activation in the presence of Wingless signalling and repression in its absence. Wingless signalling is required for the correct expression of decapentaplegic (dpp), a Transforming Growth Factor (beta) family member, in parasegments 3 and 7 of the Drosophila visceral mesoderm. Here we demonstrate that a dpp enhancer element, which directs expression of a reporter gene in the visceral mesoderm in a pattern indistinguishable from dpp, has two functional dTcf binding sites. Mutations that reduce or eliminate Wingless signalling abolish dpp reporter gene expression in parasegment 3 and reduce it in parasegment 7 while ectopic expression of Wingless signalling components expand reporter gene expression anteriorly in the visceral mesoderm. However, mutation of the dTcf binding sites in the dpp enhancer results in ectopic expression of reporter gene expression throughout the visceral mesoderm, with no diminution of expression in the endogenous sites of expression. These results demonstrate that the primary function of dTcf binding to the dpp enhancer is repression throughout the visceral mesoderm and that activation by Wingless signalling is probably not mediated via these dTcf binding sites to facilitate correct dpp expression in the visceral mesoderm.},
  issn = {0950-1991},
  url = {http://dev.biologists.org/content/127/17/3695},
  eprint = {http://dev.biologists.org/content/127/17/3695.full.pdf},
  journal = {Development},
}


@article{Yang_2000,
  author = {Yang, X. and van Beest, M. and Clevers, H. and Jones, T. and Hursh, D.A. and Mortin, M.A.},
  title = {{decapentaplegic is a direct target of dTcf repression in the Drosophila visceral mesoderm}},
  volume = {127},
  number = {17},
  pages = {3695--3702},
  year = {2000},
  publisher = {The Company of Biologists Ltd},
  abstract = {Drosophila T cell factor (dTcf) mediates transcriptional activation in the presence of Wingless signalling and repression in its absence. Wingless signalling is required for the correct expression of decapentaplegic (dpp), a Transforming Growth Factor (beta) family member, in parasegments 3 and 7 of the Drosophila visceral mesoderm. Here we demonstrate that a dpp enhancer element, which directs expression of a reporter gene in the visceral mesoderm in a pattern indistinguishable from dpp, has two functional dTcf binding sites. Mutations that reduce or eliminate Wingless signalling abolish dpp reporter gene expression in parasegment 3 and reduce it in parasegment 7 while ectopic expression of Wingless signalling components expand reporter gene expression anteriorly in the visceral mesoderm. However, mutation of the dTcf binding sites in the dpp enhancer results in ectopic expression of reporter gene expression throughout the visceral mesoderm, with no diminution of expression in the endogenous sites of expression. These results demonstrate that the primary function of dTcf binding to the dpp enhancer is repression throughout the visceral mesoderm and that activation by Wingless signalling is probably not mediated via these dTcf binding sites to facilitate correct dpp expression in the visceral mesoderm.},
  issn = {0950-1991},
  url = {http://dev.biologists.org/content/127/17/3695},
  eprint = {http://dev.biologists.org/content/127/17/3695.full.pdf},
  journal = {Development},
}


@article{Lockwood_2016,
  doi = {10.15200/winn.146723.36330},
  url = {https://doi.org/10.15200%2Fwinn.146723.36330},
  publisher = {The Winnower},
  author = {Gwilym Lockwood},
  year = {2016},
  title = {{Academic clickbait: articles with positively-framed titles, interesting phrasing, and no wordplay get more attention online.}},
}


@article{Plaven-Sigray119370,
  author = {Plav{\'e}n-Sigray, Pontus and Matheson, Granville James and Schiffler, Bj{\"o}rn Christian and Thompson, William Hedley},
  title = {{The Readability Of Scientific Texts Is Decreasing Over Time}},
  year = {2017},
  doi = {10.1101/119370},
  publisher = {Cold Spring Harbor Labs Journals},
  abstract = {Clarity and accuracy of reporting are fundamental to the scientific process. The understandability of written language can be estimated using readability formulae. Here, in a corpus consisting of 707 452 scientific abstracts published between 1881 and 2015 from 122 influential biomedical journals, we show that the readability of science is steadily decreasing. Further, we demonstrate that this trend is indicative of a growing usage of general scientific jargon. These results are concerning for scientists and for the wider public, as they impact both the reproducibility and accessibility of research findings.},
  url = {http://biorxiv.org/content/early/2017/03/28/119370},
  eprint = {http://biorxiv.org/content/early/2017/03/28/119370.full.pdf},
  journal = {bioRxiv},
}


@article{Vinkers_2015,
  doi = {10.1136/bmj.h6467},
  url = {https://doi.org/10.1136%2Fbmj.h6467},
  year = {2015},
  month = {dec},
  publisher = {{BMJ}},
  pages = {h6467},
  author = {Christiaan H Vinkers and Joeri K Tijdink and Willem M Otte},
  title = {{Use of positive and negative words in scientific {PubMed} abstracts between 1974 and 2014: retrospective analysis}},
  journal = {{BMJ}},
}
