TY - JOUR
T1 - P1/HC-Pro, a viral suppressor of RNA silencing, interferes with Arabidopsis development and miRNA function
AU - Kasschau, Kristin D.
AU - Xie, Zhixin
AU - Allen, Edwards
AU - Llave, Cesar
AU - Chapman, Elisabeth J.
AU - Krizan, Kate A.
AU - Carrington, James C.
N1 - Funding Information:
We thank Valerie Lynch-Holm and the Washington State University Electron Microscopy Center for SEM analysis, Brenda Shaffer for assistance with data analysis, and Adam Gustafson for the small RNA database. This work was supported by grants from the National Science Foundation (MCB-0209836), National Institutes of Health (AI43288), and the U.S. Department of Agriculture (NRI 2002-35319-11560). C.L. received a fellowship from the Ministerio de Educación y Cultura (Spain).
PY - 2003/2/1
Y1 - 2003/2/1
N2 - The molecular basis for virus-induced disease in plants has been a long-standing mystery. Infection of Arabidopsis by Turnip mosaic virus (TuMV) induces a number of developmental defects in vegetative and reproductive organs. We found that these defects, many of which resemble those in miRNA-deficient dicer-like1 (dcl1) mutants, were due to the TuMV-encoded RNA-silencing suppressor, P1/HC-Pro. Suppression of RNA silencing is a counterdefensive mechanism that enables systemic infection by TuMV. The suppressor interfered with the activity of miR171 (also known as miRNA39), which directs cleavage of several mRNAs coding for Scarecrow-like transcription factors, by inhibiting miR171-guided nucleolytic function. Out of ten other mRNAs that were validated as miRNA-guided cleavage targets, eight accumulated to elevated levels in the presence of P1/HC-Pro. The basis for TuMV- and other virus-induced disease in plants may be explained, at least partly, by interference with miRNA-controlled developmental pathways that share components with the antiviral RNA-silencing pathway.
AB - The molecular basis for virus-induced disease in plants has been a long-standing mystery. Infection of Arabidopsis by Turnip mosaic virus (TuMV) induces a number of developmental defects in vegetative and reproductive organs. We found that these defects, many of which resemble those in miRNA-deficient dicer-like1 (dcl1) mutants, were due to the TuMV-encoded RNA-silencing suppressor, P1/HC-Pro. Suppression of RNA silencing is a counterdefensive mechanism that enables systemic infection by TuMV. The suppressor interfered with the activity of miR171 (also known as miRNA39), which directs cleavage of several mRNAs coding for Scarecrow-like transcription factors, by inhibiting miR171-guided nucleolytic function. Out of ten other mRNAs that were validated as miRNA-guided cleavage targets, eight accumulated to elevated levels in the presence of P1/HC-Pro. The basis for TuMV- and other virus-induced disease in plants may be explained, at least partly, by interference with miRNA-controlled developmental pathways that share components with the antiviral RNA-silencing pathway.
UR - http://www.scopus.com/inward/record.url?scp=0037320231&partnerID=8YFLogxK
U2 - 10.1016/S1534-5807(03)00025-X
DO - 10.1016/S1534-5807(03)00025-X
M3 - Article
C2 - 12586064
AN - SCOPUS:0037320231
VL - 4
SP - 205
EP - 217
JO - Developmental Cell
JF - Developmental Cell
SN - 1534-5807
IS - 2
ER -