عنوان

Molecular basis for the cachexia disease syndrome of citrus

Number

TLpq304353782

.Language of Text, Soundtrack etc

انگلیسی

Title Proper

Molecular basis for the cachexia disease syndrome of citrus

General Material Designation

[Thesis]

First Statement of Responsibility

K. Reanwarakorn

Subsequent Statement of Responsibility

J. S. Semancik

Name of Publisher, Distributor, etc.

University of California, Riverside

Date of Publication, Distribution, etc.

1997

Specific Material Designation and Extent of Item

161

Dissertation or thesis details and type of degree

Ph.D.

Body granting the degree

University of California, Riverside

Text preceding or following the note

1997

Text of Note

Citrus viroid group II with 295-302 nts, consists of cachexia-inducing variants, CVd-IIb (Citrus cachexia viroid, CCaVd), CVd-IIc, Ca-903, Ca-909 and a single non-cachexia inducing variant, CVd-IIa. Parson's special mandarin (PSM) expressed gumming and stem pitting when inoculated only with cachexia-inducing variants. CVd-IIa infection resulted in strong symptoms of short internodes and rugous leave on luffa (Luffa aegyptiaca) while cachexia variants induced mild symptoms. Cachexia-inducing variants, CVd-IIb and CVd-IIc produced classical cachexia type symptoms of gumming and stem pitting on PSM, Orlando tangelo (OT) and Citrus macrophylla. However, Palestine sweet lime (PSL), the indicator of xyloporosis, displayed a simple fine pitting reaction with infection by both CVd-IIb and CVd-IIc. The nucleotide sequence of CVd-IIc although differing from CVd-IIb was identical with a variant common to xyloporosis sources from Israel. Thus, these studies suggest that cachexia and xyloporosis should be concluded as the same disease. The group II citrus viroids are characterized by a very conservative genome since only a few base changes were detected after passaging through the four different families of plants known to be hosts of hop stunt viroid (HSVd). Five variants from naturally-infected grapevine have been found and determined to contain in 295-297 bases. One HSVd-gVl, was negative for cachexia symptoms on PSM, but induced mild symptoms on PSM, but induced mild symptoms on Mapo tangelo what might represent a more sensitive indexing host than PSM. Chimeric viroid cDNA clones carrying the C-V-T2 domain region from IIa-clone induced severe symptoms on luffa, while clones with a similar genome region from IIb-clone induced very strong cachexia symptoms on PSM. In site-directed mutated cDNA clones, the six mutagenic loci introduced into the V-domain of the IIa-clone were successful in the induction of pathogenicity on PSM. From this, the C-V-T2 domains of CVd-IIa and CVd-IIb represent an important locus for regulating pathogenicity on both luffa and PSM. Probe CX2 designated as a complementary to CVd-IIb at position 182-208 was demonstrated to function as a cachexia-specific probe. The sequence as contain in the probe CX2 was tested as a cachexia specific primer for RT-PCR as both a cDNA and hDNA. When the CX2 sequence was used as a hDNA primer, a cachexia-specific product resulted under specific conditions of 1.0 mM MgCl2 at 55C.

Biological sciences

Botany

Plant pathology

J. S. Semancik

K. Reanwarakorn

Electronic name

p

[Thesis]

276903

a

Y