Evidence map›Paper›PMID 25558827›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Regulation of zygotic genome activation and DNA damage checkpoint acquisition at the mid-blastula transition.

Maomao Zhang, Priyanka Kothari, Mary Mullins, Michael A Lampson

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Regulation of zygotic genome activation by the nucleocytoplasmic ratio.Frontiers in cell and developmental biology · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Collective effects of cell cleavage dynamics.Frontiers in cell and developmental biology · 2024
    Review
  11. Article
  12. Review
  13. DNA repair genes play a variety of roles in the development of fish embryos.Frontiers in cell and developmental biology · 2023
    Review
  14. Review
  15. Review
  16. Review
  17. Cytokinetic abscission is part of the midblastula transition in early zebrafish embryogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Maomao Zhanga Department of Biology and.
Priyanka Kothari
Mary Mullins
Michael A Lampson
Philadelphia University · USUniversity of Pennsylvania · US

Funding

TRAINING PROGRAM IN DEVELOPMENTAL BIOLOGYT32HD007516 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI RAPER, JONATHAN A · 1998 to 2012
$5.6M
Regulation of cell division by mitotic kinasesR01GM083988 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GRISHCHUK, EKATERINA L, LAMPSON, MICHAEL · 2008 to 2017
$3.2M
NICHD NIH HHS T32HD007516NIGMS NIH HHS GM083988NIGMS NIH HHS R01 GM083988
6 · The paper itself

Abstract

Following fertilization, oviparous embryos undergo rapid, mostly transcriptionally silent cleavage divisions until the mid-blastula transition (MBT), when large-scale developmental changes occur, including zygotic genome activation (ZGA) and cell cycle remodeling, via lengthening and checkpoint acquisition. Despite their concomitant appearance, whether these changes are co-regulated is unclear. Three models have been proposed to account for the timing of (ZGA). One model implicates a threshold nuclear to cytoplasmic (N:C) ratio, another stresses the importance cell cycle elongation, while the third model invokes a timer mechanism. We show that precocious Chk1 activity in pre-MBT zebrafish embryos elongates cleavage cycles, thereby slowing the increase in the N:C ratio. We find that cell cycle elongation does not lead to transcriptional activation. Rather, ZGA slows in parallel with the N:C ratio. We show further that the DNA damage checkpoint program is maternally supplied and independent of ZGA. Although pre-MBT embryos detect damage and activate Chk2 after induction of DNA double-strand breaks, the Chk1 arm of the DNA damage response is not activated, and the checkpoint is nonfunctional. Our results are consistent with the N:C ratio model for ZGA. Moreover, the ability of precocious Chk1 activity to delay pre-MBT cell cycles indicate that lack of Chk1 activity limits checkpoint function during cleavage cycles. We propose that Chk1 gain-of-function at the MBT underlies cell cycle remodeling, whereas ZGA is regulated independently by the N:C ratio.

Indexed as

GenomeAnimalsBlastulaCell Cycle CheckpointsCheckpoint Kinase 1Checkpoint Kinase 2DNA Breaks, Double-StrandedDNA RepairEmbryo, NonmammalianGamma RaysHistonesHydroxyureaProtein KinasesRecombinant Fusion ProteinsSignal TransductionZebrafishCheckpoint Kinase 1Checkpoint Kinase 2HistonesHydroxyureaProtein KinasesRecombinant Fusion ProteinsZebrafish Proteinscell cycle checkpointsembryogenesisMBT, Mid-blastula Transitionmid-blastula transitionZGA, Zygotic genome activationzygotic genome activation

Identifiers

PMID25558827
PMCPMC4614548
OpenAlexW2075899471

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.