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. 2015 Mar 31;12(3):255–267. doi: 10.1080/15476286.2015.1017221

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© Wen-An Pan, Hsin-Yue Tsai, Shun-Chang Wang, Michael Hsiao, Pei-Yu Wu, and Ming-Daw Tsai

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 4. — Identification of specific residues responsible for the RRM function in rRNA processing and G1 progression. (A) Sequence alignment of NIFK-RRM orthologues from different species. Asterisks indicate residues selected for alanine substitution. (B) Cell cycle analyses, (C) nascent rRNA synthesis, and (D) Western blot analyses of the phenotypically rescued cells described in Fig. 3, showing defects of NIFK-RRM mutants in rescuing NIFK silencing. The asterisk indicates ectopic NIFK and the arrow, endogenous NIFK.