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In developmental biology, midblastula or midblastula transition (MBT) is a stage during the blastula stage of embryonic development in which zygotic gene transcription is activated. There are three major characteristics of pre-MBT embryos. Firstly, all of the embryonic cells undergo cell division at the same time.[1] Secondly, zygotic chromatin is condensed, hypo-acetylated and H3 methylated,[2] indicating that most of the genes are in a repressed heterochromatic state. Finally, embryos are observed to translate only maternally inherited mRNA, i.e. that mRNA which is present in the oocyte when it is fertilised.[3] The mRNA is localised in different parts of the oocyte, so that as the embryo divides it is segregated into different cells. This segregation is thought to underlie much of the differentiation of cells that occurs after MBT. Once MBT has taken place, the embryo begins to transcribe its own DNA, cells become motile and cell division becomes asynchronous. Since the cells are now transcribing their own DNA, this stage is where differential expression of paternal genes is first observed.


The timing of MBT varies between different organisms. Zebrafish MBT occurs at cycle 10,[4] whilst it occurs at cycle 13 in both Xenopus and Drosophila. Cells are thought to time the MBT by measuring the nucleocytoplasmic ratio, which is effectively the ratio between the volume of cytosol and the amount of DNA. Evidence for this hypothesis comes from the observation that the timing of MBT can be sped up by adding extra DNA,[5] or by halving the amount of cytoplasm.[6] The exact method by which the cell achieves this control is unknown, but it is thought to involve a cytosolic protein. In Drosophila, the zinc-finger transcription factor Zelda is bound to regulatory regions of genes expressed by the zygote,[7] and in zebrafish, the homeodomain protein Pou5f1 (an ortholog of mammalian Oct4) has an analogous role.[8] Without the function of these proteins MBT gene expression synchrony is disrupted, but particular mechanisms of coordinating the timing of gene expression are under investigation.


  1. ^ Masui Y, Wang P (1998). "Cell cycle transition in early embryonic development of Xenopus laevis" (PDF). Biol. Cell. 90 (8): 537–548. PMID 10068998. doi:10.1016/S0248-4900(99)80011-2. 
  2. ^ Meehana R, Dunicana D, Ruzova A, Pennings S (2005). "Epigenetic silencing in embryogenesis". Exp. Cell Biol. 309 (2): 241–249. PMID 16112110. doi:10.1016/j.yexcr.2005.06.023. 
  3. ^ Sibon O, Stevenson V, Theurkauf W (1997). "DNA-replication checkpoint control at the Drosophila midblastula transition". Nature. 388 (6637): 93–97. PMID 9214509. doi:10.1038/40439. 
  4. ^ Kane D, Kimmel C (1993). "The zebrafish midblastula transition". Development. 119 (2): 447–456. PMID 8287796. 
  5. ^ Mita I, Obata C (1984). "Timing of early morphogenetic events in tetraploid starfish embryos". J. Exp. Zool. 229 (2): 215–222. doi:10.1002/jez.1402290206. 
  6. ^ Mita I (1983). "Studies on factors affecting the timing of early morphogenetic events during starfish embryogenesis". J. Exp. Zool. 225 (2): 293–9. doi:10.1002/jez.1402250212. 
  7. ^ Harrison, MM; Li, XY; Kaplan, T; Botchan, MR; Eisen, MB (Oct 2011). "Zelda binding in the early Drosophila melanogaster embryo marks regions subsequently activated at the maternal-to-zygotic transition". PLoS Genet. 7 (10): e1002266. doi:10.1371/journal.pgen.1002266. 
  8. ^ Leichsenring, M; Maes, J; Mössner, R; Driever, W; Onichtchouk, D (2013). "Pou5f1 transcription factor controls zygotic gene activation in vertebrates". Science. 341 (6149): 1005–9. PMID 23950494. doi:10.1126/science.1242527.