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Overexpression of TOR (target of rapamycin) inhibits cell proliferation in Dictyostelium discoideum
Author(s) -
Swer Pynskhem Bok,
Mishra Himanshu,
Lohia Rakhee,
Saran Shweta
Publication year - 2016
Publication title -
journal of basic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.58
H-Index - 54
eISSN - 1521-4028
pISSN - 0233-111X
DOI - 10.1002/jobm.201500313
Subject(s) - dictyostelium discoideum , biology , gene knockdown , tor signaling , microbiology and biotechnology , cell growth , rna interference , mutant , cell culture , kinase , gene , rna , biochemistry , genetics
TOR (target of rapamycin) protein kinase acts as a central controller of cell growth and development of an organism. Present study was undertaken to find the expression pattern and role of TOR during growth and development of Dictyostelium discoideum . Failures to generate either knockout and/or knockdown mutants indicate that interference with its levels led to cellular defects. Thus, the effects of TOR (DDB_G0281569) overexpression specifically, cells expressing Dd(Δ211‐TOR)‐Eyfp mutant was analyzed. Elevated expression of (Δ211‐TOR)‐Eyfp reduced both cell size and cell proliferation. DdTOR was found to be closer to fungus. mRNA level of TOR was found maximally in the freshly starved/aggregate cells that gradually declined. This was also strengthened by the expression patterns observed by in situ and the analysis of β‐galactosidase reporter driven by the putative TOR promoter. The TOR protein was found to be highest at the aggregate stage. The fusion protein, (Δ211‐TOR)‐Eyfp was localized to the cell membrane, cytosol, and the nucleus. We suggest, DdTOR to be an essential protein and high TOR expression inhibits cell proliferation.