INVESTIGADORES
ASURMENDI Sebastian
artículos
Título:
Infection and coaccumulation of tobacco mosaic virus proteins alter microRNA levels, correlating with symptom and plant development.
Autor/es:
BAZZINI AA; HOPP HE; BEACHY RN; ASURMENDI S
Revista:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Referencias:
Año: 2007 vol. 104 p. 12157 - 12162
ISSN:
0027-8424
Resumen:
Infections by plant virus generally cause disease symptoms by
interfering with cellular processes. Here we demonstrated that
infection of Nicotiana tabacum (N.t) by plant viruses representative
of the Tobamoviridae, Potyviridae, and Potexviridae families altered
accumulation of certain microRNAs (miRNAs). A correlation
was observed between symptom severity and alteration in levels
of miRNAs 156, 160, 164,166, 169, and 171 that is independent of
viral posttranscriptional gene silencing suppressor activity. Hybrid
transgenic plants that produced tobacco mosaic virus (TMV) movement
protein (MP) plus coat protein (CP)T42W (a variant of CP)
exhibited disease-like phenotypes, including abnormal plant development.
Grafting studies with a plant line in which both
transgenes are silenced confirmed that the disease-like phenotypes
are due to the coexpression of CP and MP. In hybrid
MPxCPT42W plants and TMV-infected plants, miRNAs 156, 164, 165,
and 167 accumulated to higher levels compared with nontransgenic
and noninfected tissues. Bimolecular fluorescence complementation
assays revealed that MP interacts with CPT42W in vivoNicotiana tabacum (N.t) by plant viruses representative
of the Tobamoviridae, Potyviridae, and Potexviridae families altered
accumulation of certain microRNAs (miRNAs). A correlation
was observed between symptom severity and alteration in levels
of miRNAs 156, 160, 164,166, 169, and 171 that is independent of
viral posttranscriptional gene silencing suppressor activity. Hybrid
transgenic plants that produced tobacco mosaic virus (TMV) movement
protein (MP) plus coat protein (CP)T42W (a variant of CP)
exhibited disease-like phenotypes, including abnormal plant development.
Grafting studies with a plant line in which both
transgenes are silenced confirmed that the disease-like phenotypes
are due to the coexpression of CP and MP. In hybrid
MPxCPT42W plants and TMV-infected plants, miRNAs 156, 164, 165,
and 167 accumulated to higher levels compared with nontransgenic
and noninfected tissues. Bimolecular fluorescence complementation
assays revealed that MP interacts with CPT42W in vivoTobamoviridae, Potyviridae, and Potexviridae families altered
accumulation of certain microRNAs (miRNAs). A correlation
was observed between symptom severity and alteration in levels
of miRNAs 156, 160, 164,166, 169, and 171 that is independent of
viral posttranscriptional gene silencing suppressor activity. Hybrid
transgenic plants that produced tobacco mosaic virus (TMV) movement
protein (MP) plus coat protein (CP)T42W (a variant of CP)
exhibited disease-like phenotypes, including abnormal plant development.
Grafting studies with a plant line in which both
transgenes are silenced confirmed that the disease-like phenotypes
are due to the coexpression of CP and MP. In hybrid
MPxCPT42W plants and TMV-infected plants, miRNAs 156, 164, 165,
and 167 accumulated to higher levels compared with nontransgenic
and noninfected tissues. Bimolecular fluorescence complementation
assays revealed that MP interacts with CPT42W in vivoT42W (a variant of CP)
exhibited disease-like phenotypes, including abnormal plant development.
Grafting studies with a plant line in which both
transgenes are silenced confirmed that the disease-like phenotypes
are due to the coexpression of CP and MP. In hybrid
MPxCPT42W plants and TMV-infected plants, miRNAs 156, 164, 165,
and 167 accumulated to higher levels compared with nontransgenic
and noninfected tissues. Bimolecular fluorescence complementation
assays revealed that MP interacts with CPT42W in vivoT42W plants and TMV-infected plants, miRNAs 156, 164, 165,
and 167 accumulated to higher levels compared with nontransgenic
and noninfected tissues. Bimolecular fluorescence complementation
assays revealed that MP interacts with CPT42W in vivoT42W in vivo
and leads to the hypothesis that complexes formed between MP
and CP caused increases in miRNAs that result in disease symptoms.
This work presents evidence that virus infection and viral proteins
influence miRNA balance without affecting posttranscriptional
gene silencing and contributes to the hypothesis that viruses
exploit miRNA pathways during pathogenesis.