Michael Lichten

  • National Cancer Institute
ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-9707-2956

Annotations

  1. Peer Review: New initiatives to enhance the value of eLife’s process
    One of these manuscripts was withdrawn prior to publication

    I actually was the editor at PLOS Genetics who handled this paper, under an eLife-PLOS manuscript transfer mechanism. Based on the eLife reviews, I returned the ms to authors for revision. This prompted them to refine the data analysis, leading to modified but much stronger conclusions that, in my opinion, made the paper a much stronger contribution that publishing the original ms with critical reviews would have been. My point? Sometimes the review process actually improves papers! I am concerned that this would not have happened if the authors had decided to stick with eLife--they might not have been so motivated to do the hard work of reanalysis that made the paper stronger.

  2. Point of View: Four erroneous beliefs thwarting more trustworthy research
    Suggestions to help build cultures and climates that assure deserved trust

    While the reviews and response mention teaching and training to a greater extent, there is a lamentable absence of substantial discussion of this critical issue in the current article. The current article seems, to me, analogous to deciding to decrease traffic accidents by promulgating more driving regulations and increasing enforcement, while ignoring the content and quality of instruction of student drivers. The current emphasis on a single course on research integrity does little, if anything to address this serious deficit in our current system of education, and I am sorry that this article ignored the problem almost entirely

  3. No title available

    This work has now been extended to examine MLH3-dependence of VDE-initiated crossovers in the same recombination reporter inserted at six additional loci (Shodhan, Medhi and Lichten, https://doi.org/10.1534/g3.119.400150). The original experimental conclusions, that VDE-initiated crossovers are MLH3-dependent at HIS4, and are MLH3-independent at URA3, were confirmed. VDE-initiated crossovers at all six additional insert loci were also found to be MLH3-independent, though at these loci MLH3-independence was not related to regional Hop1 enrichment. There were also no discernible influences of chromosome size, or locus proximity to centromere or telomere. The hypothesis put forward in the original paper, that local Hop1-enrichment determines the MLH3-dependence of crossovers, is not supported by the general MLH3-independence of VDE-initiated crossovers. VDE-initiated crossovers at the six additional loci, like those at HIS4 and URA3, become partially MLH3-dependent in pch2 mutants, confirming the generality of that original observation. We currently do not understand the exceptional MLH3-dependence of VDE-initiated crossovers at HIS4. We cannot rule out the possibility that factors in addition to Hop1 enrichment are required, or that Hop1 enrichment is indirectly associated with other factors that directly determine the MLH3-dependence or independence of VDE-initiated crossovers. The latter suggestion stands in contrast to published findings suggesting the direct involvement of meiotic chromosome axis proteins, including Hop1, in the major pathway for Spo11-initiated meiotic crossovers, which are MLH3-dependent (De Muyt, A., et al., https://doi:10.1101/gad.308510.117; Serrentino, M.E., et al., https://doi:10.1371/journal.pgen.1003416).