Pathogenicity of Alternanthera mosaic virus is affected by determinants in RNA-dependent RNA polymerase and by reduced efficacy of silencing suppression in a movement-competent TGB1

Title
Pathogenicity of Alternanthera mosaic virus is affected by determinants in RNA-dependent RNA polymerase and by reduced efficacy of silencing suppression in a movement-competent TGB1
Author(s)
임현섭[임현섭]아나 마리아 바이라[아나 마리아 바이라]마이틀 라인셀[마이틀 라인셀]배한홍브라이언 베일리[브라이언 베일리]레슬리 도마이어[레슬리 도마이어]존 해몬드[존 해몬드]
Keywords
SINGLE AMINO-ACID; NICOTIANA-BENTHAMIANA; NUCLEOTIDE-SEQUENCE; GENETIC-STRUCTURE; CDNA-CLONES; CELL-DEATH; PROTEIN; POTEXVIRUS; HOST; TEMPERATURE
Issue Date
201001
Publisher
SOC GENERAL MICROBIOLOGY
Citation
JOURNAL OF GENERAL VIROLOGY, v.91, pp.277 - 287
Abstract
Four biologically active cDNA clones were derived from the Alternanthera mosaic virus (AltMV; genus Potexvirus) isolate, AltMV-SP, which differ in symptoms in infected Nicotiana benthamiana plants. Two clones induced necrosis and plant death; a mixture of all four clones induced milder symptoms than AltMV-SP. Replication of all clones was enhanced by a minimum of fourfold at 15 degrees C. A mixture of clones 4-7 (severe) and 3-1 (mild) was indistinguishable from AltMV-SP, but the ratio of 4-7 to 3-1 differed at 25 and 15 degrees C. RNA copy numbers of mixed infections were always below those of 4-7 alone. Determinants of symptom severity were identified in both Pol and TGB1; the mildest (4-1) and most severe (3-7) clones differed at three residues in the 'core' Pol domain [R(1110)P, K(11121)R, R(11255)K] and one [S(1535)P] in the C-terminal Pol domain of RNA-dependent RNA polymerase, and one in TGB1 [P(88)L].Pol[P(1110),R(1121),K(1255)]+TGB1(L(88))] always induced systemic necrosis at 15 degrees C. Gene exchanges of Pol and TGB1 each affected replication and symptom expression, with TGB1(P(88)) significantly reducing silencing suppression. The difference in silencing suppression between TGB1(P(88)) and TGB1(L(88)) was confirmed by an agroinfiltration assay. Further, co-expression of TGB1(P(88)) and TGB1(L(138)) resulted in interference in the suppression of silencing by TGB1(L(88)). Yeast two-hybrid analysis confirmed that TGB1(P(88)) and TGB(1L(88)) interact. These results identify a TGB1 residue that significantly affects replication and silencing suppression, but maintains full movement functions.
URI
http://hdl.handle.net/YU.REPOSITORY/22986http://dx.doi.org/10.1099/vir.0.014977-0
ISSN
0022-1317
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