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Meiomitosis

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In cell biology, Meiomitosis is an aberrant cellular division pathway that combines normal mitosis pathways with ectopically expressed meiotic machinery resulting in genomic instability.[1]

Description

Meiotic pathways are normally restricted to germ cells. Meiotic proteins drive double stranded DNA breaks, chiasma formation, sister chromatid adhesion and rearrange the spindle apparatus.[2]  

During meiosis, there are 2 sets of cell divisions, the second division is similar to mitosis in that sister chromatids are directly separated.  However, in the first meiotic division the sister chromatids are held together by cohesins and segregated from their homologous pair of cohesion bound sister chromatids after resolution of recombination crossover points (chiasma) between the homologous pairs.  The collision of mitosis and meiosis (first division) pathways could cause abnormal chiasma formation, abnormal cohesion expression, and mitotic/meiotic spindle defects that could result in insertions, deletions, abnormal segregation, DNA bridging, and potentially failure of cell division altogether resulting in polyploidy.

Role in cancer

Meiotic proteins have been noted to be expressed in cancer particularly melanoma[3] and lymphoma. In cutaneous T-cell lymphoma meiosis proteins have been shown to be regulated with the cell cycle.[4]  Lymphoma cell lines have also been noted to up-regulate meiosis specific genes with irradiation and a correlation with mitotic arrest and polyploidy has been noted.[5]  The overall role of meiomitosis in cancer development and evolution has yet to be determined.

References

  1. ^ Grichnik, James M. (October 2008). "Melanoma, nevogenesis, and stem cell biology". The Journal of Investigative Dermatology. 128 (10): 2365–2380. doi:10.1038/jid.2008.166. ISSN 1523-1747. PMID 18787546.
  2. ^ Ross, Andrew L.; Leder, Daniel E.; Weiss, Jonathan; Izakovic, Jan; Grichnik, James M. (September 2011). "Genomic instability in cultured stem cells: associated risks and underlying mechanisms". Regenerative Medicine. 6 (5): 653–662. doi:10.2217/rme.11.44. ISSN 1746-076X. PMID 21916599.
  3. ^ Lindsey, Scott F.; Byrnes, Diana M.; Eller, Mark S.; Rosa, Ashley M.; Dabas, Nitika; Escandon, Julia; Grichnik, James M. (2013). "Potential role of meiosis proteins in melanoma chromosomal instability". Journal of Skin Cancer. 2013: 190109. doi:10.1155/2013/190109. ISSN 2090-2905. PMC 3694528. PMID 23840955.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Tsang, Matthew; Gantchev, Jennifer; Netchiporouk, Elena; Moreau, Linda; Ghazawi, Feras M.; Glassman, Steven; Sasseville, Denis; Litvinov, Ivan V. (2018-12-28). "A study of meiomitosis and novel pathways of genomic instability in cutaneous T-cell lymphomas (CTCL)". Oncotarget. 9 (102): 37647–37661. doi:10.18632/oncotarget.26479. ISSN 1949-2553. PMC 6340880. PMID 30701021.
  5. ^ Kalejs, Martins; Ivanov, Andrey; Plakhins, Gregory; Cragg, Mark S.; Emzinsh, Dzintars; Illidge, Timothy M.; Erenpreisa, Jekaterina (2006-01-09). "Upregulation of meiosis-specific genes in lymphoma cell lines following genotoxic insult and induction of mitotic catastrophe". BMC Cancer. 6: 6. doi:10.1186/1471-2407-6-6. ISSN 1471-2407. PMC 1351196. PMID 16401344.{{cite journal}}: CS1 maint: unflagged free DOI (link)

Sources


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