Mutational Analysis of the Coat Protein Geneof Brome Mosaic Virus: Effects on Replication andMovement in Barley and in Chenopodium hybridum. Stanislaw Flasinski. Plant Molecular Biology Center and Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, U.S.A. Aleksandra Dzianott, Steven Pratt, and Jozef J. Bujarski. Plant Molecular Biology Center and Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, U.S.A. Received 10 June 1994. MPMI 8:23-31. Accepted 24 October 1994. Copyright 1995 The American Phytopathological Society.

The coat protein (CP) open reading frame (ORF) of brome mosaic virus (BMV) has been mutated to study host-related CP functions in barley, a systemic host, and in Chenopodium hybridum L. which supports both local lesion formation and systemic spread of BMV. To test the role of the N-terminal region of CP, mutants Cl to C3, which synthesized the CP lacking first seven amino acids, and mutant Dl, which had Trp 22 and Thr 23 replaced with Phe-Gly-Ser, were generated. Cl to C3 inhibited virus systemic spread in C. hybridum but not in barley while Dl only reduced virus accumulation in noninoculated leaves of C. hybridum. More internal CP regions were tested by mutation of Lys 63 to Leu (mutant SP3) and Lys 129 to Arg (mutant SP1). SP1 behaved similarly to Cl to C3 while SP3 similarly to Dl. In addition, SP3 reduced concentrations of RNA3 and RNA4 in both hosts. Apparently, various CP regions differentially affect, either directly or indirectly, virus translocation in different hosts, suggesting both the CP and host factors to be important for virus spread. Larger deletions in the CP ORF (mutants BB4 and SX1) or a decrease of CP production by using a frameshift mutant C, inhibited virus systemic spread in both hosts, and delayed the appearance of smaller local lesions on C. hybridum. Thus, the CP is not required for cell-to-cell movement but is required for systemic translocation of BMV.