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. Author manuscript; available in PMC: 2018 Jun 25.

Published in final edited form as: Virology. 2015 May 15;483:149–162. doi: 10.1016/j.virol.2015.04.002

FIG. 5 — In vivo SELEX of satC19. (A) Results of five rounds of passaging satC with 19 random bases replacing H2 (satC19). Sequences related to the four distinct “winning” satCs (samples FF_q, GG_q, HH_q, and II_q) are boxed. Underlined nt denote differences between related satC clones. Second-site mutations are identified by symbols and defined at the bottom of the figure. (B-D) Models for sequence expansion in DD_q, II_q, and HH_q. (E) Secondary structure models for the 5′ region of SELEX winners FF_q, GG_q, HH_q and II_q. Results of SHAPE structure probing are shown on the model of HH_q (see Fig. 1B for nucleotide coloring). Boxed nucleotides in GG_q and HH_q denote second-site mutations.

FIG. 5 — In vivo SELEX of satC19. (A) Results of five rounds of passaging satC with 19 random bases replacing H2 (satC19). Sequences related to the four distinct “winning” satCs (samples FF_q, GG_q, HH_q, and II_q) are boxed. Underlined nt denote differences between related satC clones. Second-site mutations are identified by symbols and defined at the bottom of the figure. (B-D) Models for sequence expansion in DD_q, II_q, and HH_q. (E) Secondary structure models for the 5′ region of SELEX winners FF_q, GG_q, HH_q and II_q. Results of SHAPE structure probing are shown on the model of HH_q (see Fig. 1B for nucleotide coloring). Boxed nucleotides in GG_q and HH_q denote second-site mutations.