Open Access
Proteomic and protein interaction network analysis of human T lymphocytes during cell‐cycle entry
Author(s) -
Orr Stephen J,
Boutz Daniel R,
Wang Rong,
Chronis Constantinos,
Lea Nicholas C,
Thayaparan Thivyan,
Hamilton Emma,
Milewicz Hanna,
Blanc Eric,
Mufti Ghulam J,
Marcotte Edward M,
Thomas N Shaun B
Publication year - 2012
Publication title -
molecular systems biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 8.523
H-Index - 148
ISSN - 1744-4292
DOI - 10.1038/msb.2012.5
Subject(s) - biology , microbiology and biotechnology , cell cycle , ribosome biogenesis , effector , cell growth , chromatin , cell , biogenesis , ribosome , genetics , rna , gene
Regulating the transition of cells such as T lymphocytes from quiescence (G 0 ) into an activated, proliferating state involves initiation of cellular programs resulting in entry into the cell cycle (proliferation), the growth cycle (blastogenesis, cell size) and effector (functional) activation. We show the first proteomic analysis of protein interaction networks activated during entry into the first cell cycle from G 0 . We also provide proof of principle that blastogenesis and proliferation programs are separable in primary human T cells. We employed a proteomic profiling method to identify large‐scale changes in chromatin/nuclear matrix‐bound and unbound proteins in human T lymphocytes during the transition from G 0 into the first cell cycle and mapped them to form functionally annotated, dynamic protein interaction networks. Inhibiting the induction of two proteins involved in two of the most significantly upregulated cellular processes, ribosome biogenesis (eIF6) and hnRNA splicing (SF3B2/SF3B4), showed, respectively, that human T cells can enter the cell cycle without growing in size, or increase in size without entering the cell cycle.