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From Wikipedia, the free encyclopedia

The dictyate or dictyotene[1] is a prolonged resting phase in oogenesis. It occurs in the stage of meiotic prophase I[2] in ootidogenesis. It starts late in fetal life[2] and is terminated shortly before ovulation by the LH surge.[3] Thus, although the majority of oocytes are produced in female fetuses before birth, these pre-eggs remain arrested in the dictyate stage until puberty commences and the cells complete ootidogenesis.

In both mouse and human, oocyte DNA of older individuals has substantially more double-strand breaks than that of younger individuals.[4]

The dictyate appears to be an adaptation for efficiently removing damages in germ line DNA by homologous recombinational repair.[5] Prophase arrested oocytes have a high capability for efficient repair of DNA damages.[5] DNA repair capability appears to be a key quality control mechanism in the female germ line and a critical determinant of fertility.[5]

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Transcription

Translation halt

There are a lot of mRNAs that have been transcribed but not translated during dictyate.[6] Shortly before ovulation, the oocyte of interest activates these mRNA strains.

Biochemistry mechanism

Translation of mRNA in dictyate is partly explained by molecules binding to sites on the mRNA strain, which results in that initiation factors of translation can not bind to that site. Two such molecules, that impedes initiation factors, are CPEB and maskin, which bind to CPE (cytoplasmic polyadenylation element). When these two molecules remain together, then maskin binds the initiation factor eIF-4E,[6] and thus eIF4E can no longer interact with the other initiation factors[7] and no translation occurs. On the other hand, dissolution of the CPEB/maskin complex leads to eIF-4E binding to the initiation factor eIF-4G,[6] and thus translation starts, which contributes to the end of dictyate and further maturation of the oocyte.

See also

References

  1. ^ Boron, W.F.; Boulpaep, E.L., eds. (2005). Medical Physiology. Elsevier Saunders. ISBN 1-4160-2328-3. OCLC 56191776.
  2. ^ a b National Research Council (US) Safe Drinking Water Committee; Thomas, R. D. (1986). Thomas, Richard D (ed.). Drinking Water and Health. Vol. 6. Washington, D.C.: National Academies Press. p. 35. doi:10.17226/921. ISBN 0-309-03687-9. PMID 25032465.
  3. ^ Barresi, Michael (2006). "Hormones and Mammalian Egg Maturation". DevBio: A Companion to Developmental Biology. Archived from the original on 2008-05-08.
  4. ^ Titus S, Li F, Stobezki R, Akula K, Unsal E, Jeong K, Dickler M, Robson M, Moy F, Goswami S, Oktay K (2013). "Impairment of BRCA1-related DNA double-strand break repair leads to ovarian aging in mice and humans". Sci Transl Med. 5 (172): 172ra21. doi:10.1126/scitranslmed.3004925. PMC 5130338. PMID 23408054.
  5. ^ a b c Stringer JM, Winship A, Zerafa N, Wakefield M, Hutt K (May 2020). "Oocytes can efficiently repair DNA double-strand breaks to restore genetic integrity and protect offspring health". Proc Natl Acad Sci U S A. 117 (21): 11513–22. doi:10.1073/pnas.2001124117. PMC 7260990. PMID 32381741.
  6. ^ a b c Stebbins-Boaz B, Cao Q, de Moor CH, Mendez R, Richter JD (December 1999). "Maskin is a CPEB-associated factor that transiently interacts with elF-4E". Mol Cell. 4 (6): 1017–27. doi:10.1016/s1097-2765(00)80230-0. PMID 10635326.
  7. ^ Lodish HF, Berk A, Kaiser C, Krieger M, Scott MP, Bretscher A, Ploegh HL, Matsudaira PT (2008). Molecular cell biology (6th ed.). W.H. Freeman. p. 351. ISBN 978-0-7167-4366-8. OCLC 83758878.
This page was last edited on 2 July 2024, at 14:13
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