María R. Albiach-Martí
University of Florida
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Publication
Featured researches published by María R. Albiach-Martí.
Journal of Virology | 2000
María R. Albiach-Martí; Munir Mawassi; Siddarame Gowda; Tatineni Satyanarayana; Mark E. Hilf; Savita Shanker; Ernesto C. Almira; María C. Vives; Carmelo López; José Guerri; Ricardo Flores; Pedro Moreno; Steve M. Garnsey; William O. Dawson
ABSTRACT The first Citrus tristeza virus (CTV) genomes completely sequenced (19.3-kb positive-sense RNA), from four biologically distinct isolates, are unexpectedly divergent in nucleotide sequence (up to 60% divergence). Understanding of whether these large sequence differences resulted from recent evolution is important for the design of disease management strategies, particularly the use of genetically engineered mild (essentially symptomless)-strain cross protection and RNA-mediated transgenic resistance. The complete sequence of a mild isolate (T30) which has been endemic in Florida for about a century was found to be nearly identical to the genomic sequence of a mild isolate (T385) from Spain. Moreover, samples of sequences of other isolates from distinct geographic locations, maintained in different citrus hosts and also separated in time (B252 from Taiwan, B272 from Colombia, and B354 from California), were nearly identical to the T30 sequence. The sequence differences between these isolates were within or near the range of variability of the T30 population. A possible explanation for these results is that the parents of isolates T30, T385, B252, B272, and B354 have a common origin, probably Asia, and have changed little since they were dispersed throughout the world by the movement of citrus. Considering that the nucleotide divergence among the other known CTV genomes is much greater than those expected for strains of the same virus, the remarkable similarity of these five isolates indicates a high degree of evolutionary stasis in some CTV populations.
Journal of Virology | 2002
Tatineni Satyanarayana; Siddarame Gowda; María A. Ayllón; María R. Albiach-Martí; Shailaja Rabindran; William O. Dawson
ABSTRACT Citrus tristeza virus (CTV), a member of the Closteroviridae, has a 19.3-kb positive-stranded RNA genome that is organized into 12 open reading frames (ORFs) with the 10 3′ genes expressed via a nested set of nine or ten 3′-coterminal subgenomic mRNAs (sgRNAs). Relatively large amounts of negative-stranded RNAs complementary to both genomic and sgRNAs accumulate in infected cells. As is characteristic of RNA viruses, wild-type CTV produced more positive than negative strands, with the plus-to-minus ratios of genomic and sgRNAs estimated at 10 to 20:1 and 40 to 50:1, respectively. However, a mutant with all of the 3′ genes deleted replicated efficiently, but produced plus to minus strands at a markedly decreased ratio of 1 to 2:1. Deletion analysis of 3′-end genes revealed that the p23 ORF was involved in asymmetric RNA accumulation. A mutation which caused a frameshift after the fifth codon resulted in nearly symmetrical RNA accumulation, suggesting that the p23 protein, not a cis-acting element within the p23 ORF, controls asymmetric accumulation of CTV RNAs. Further in-frame deletion mutations in the p23 ORF suggested that amino acid residues 46 to 180, which contained RNA-binding and zinc finger domains, were indispensable for asymmetrical RNA accumulation, while the N-terminal 5 to 45 and C-terminal 181 to 209 amino acid residues were not absolutely required. Mutation of conserved cysteine residues to alanines in the zinc finger domain resulted in loss of activity of the p23 protein, suggesting involvement of the zinc finger in asymmetric RNA accumulation. The absence of p23 gene function was manifested by substantial increases in accumulation of negative-stranded RNAs and only modest decreases in positive-stranded RNAs. Moreover, the substantial decrease in the accumulation of negative-stranded coat protein (CP) sgRNA in the presence of the functional p23 gene resulted in a 12- to 15-fold increase in the expression of the CP gene. Apparently the excess negative-stranded sgRNA reduces the availability of the corresponding positive-stranded sgRNA as a messenger. Thus, the p23 protein controls asymmetric accumulation of CTV RNAs by downregulating negative-stranded RNA accumulation and indirectly increases expression of 3′ genes.
Molecular Breeding | 2004
María R. Albiach-Martí; Jude W. Grosser; Siddarame Gowda; Munir Mawassi; Tatineni Satyanarayana; Stephen M. Garnsey; William O. Dawson
Citrus tristeza virus (CTV) is the most economically important viral disease of citrus worldwide. Cultivars with improved CTV tolerance or resistance are needed to manage CTV-induced diseases. The citrus relatives Poncirus trifoliata (L.) Raf., Swinglea glutinosa (Blanco) Merr., and Severinia buxifolia (Poir) Ten. are potential sources of CTV resistance, but their resistance mechanisms are poorly characterized. As a first step to examine the mechanisms of resistance to CTV in these citrus relatives and selected Citrus × Poncirus hybrids, it was necessary to develop methods for protoplast isolation and viral inoculation to allow examination of CTV multiplication in this range of citrus varieties and relatives. Leaf and/or cultured cell protoplasts were isolated and inoculated with four biologically distinct CTV isolates. Northern-blot hybridization analyses for progeny RNAs and immuno-electron microscopy assays for newly produced virions showed that CTV replicated and produced infectious particles in protoplasts from all of the resistant plants tested. These results suggest that resistance to CTV observed at the plant level results from a lack of virus movement and/or some induced resistance response, rather than lack of viral multiplication at the cellular level.
Molecular Plant Pathology | 2008
Pedro Moreno; Silvia Ambrós; María R. Albiach-Martí; José Guerri; Leandro Peña
Virology | 2000
Tatineni Satyanarayana; Siddarame Gowda; Munir Mawassi; María R. Albiach-Martí; María A. Ayllón; Cecile J. Robertson; Stephen M. Garnsey; William O. Dawson
Proceedings of the National Academy of Sciences of the United States of America | 1999
Tatineni Satyanarayana; Siddarame Gowda; Vitaly P. Boyko; María R. Albiach-Martí; Munir Mawassi; J. Navas-Castillo; Alexander V. Karasev; Valerian V. Dolja; Mark E. Hilf; D.J. Lewandowski; Pedro Moreno; Moshe Bar-Joseph; Stephen M. Garnsey; William O. Dawson
Virology | 1997
Jesús Navas-Castillo; María R. Albiach-Martí; Siddarame Gowda; Mark E. Hilf; Stephen M. Garnsey; William O. Dawson
Virology | 2001
Tatineni Satyanarayana; Moshe Bar-Joseph; Munir Mawassi; María R. Albiach-Martí; María A. Ayllón; Siddarame Gowda; Mark E. Hilf; Pedro Moreno; Stephen M. Garnsey; William O. Dawson
Virology | 2001
Siddarame Gowda; Tatineni Satyanarayana; María A. Ayllón; María R. Albiach-Martí; Munir Mawassi; Shailaja Rabindran; Stephen M. Garnsey; William O. Dawson
Virology | 2000
Siddarame Gowda; Tatineni Satyanarayana; Craig L. Davis; Jesús Navas-Castillo; María R. Albiach-Martí; Munir Mawassi; Nikola Valkov; Moshe Bar-Joseph; Pedro Moreno; William O. Dawson