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פותח על ידי קלירמאש פתרונות בע"מ -
Sugar‐regulated susceptibility of tomato fruit to Colletotrichum and Penicillium requires differential mechanisms of pathogenicity and fruit responses
Year:
0
Source of publication :
Environmental Microbiology
Authors :
זיו, כרמית
;
.
סלע, נעה
;
.
פרוסקי, דב
;
.
קומאר, דיליפ
;
.
שפר, ארתור
;
.
Volume :
Co-Authors:

Maxim Itkin - Life Science Core Facilities, Weizmann Institute of Science, Rehovot, 7610001 Israel.
Sergey Malitsky - Life Science Core Facilities, Weizmann Institute of Science, Rehovot, 7610001 Israel
 

Facilitators :
From page:
0
To page:
0
(
Total pages:
1
)
Abstract:

Colletotrichum gloeosporioides and Penicillium expansum cause postharvest diseases in tropical and deciduous fruit. During colonization, C. gloeosporioides and P. expansum secrete ammonia in hosts with low sugar content (LowSC) and gluconic acid in hosts with high sugar content (HighSC), respectively, as a mechanism to modulate enhanced pathogenicity. We studied the pathogens interactions with tomato lines of similar genetic background but differing in their sugar content. C. gloeosporioides showed enhanced colonization of the LowSC line with differential expression response of 15% of its genes including enhanced relative expression of glycosyl hydrolases, glucanase and MFS‐transporter genes. Enhanced colonization of P. expansum occurred in the HighSC line, accompanied by an increase in carbohydrate metabolic processes mainly phosphoenolpyruvate carboxykinase, and only 4% of differentially expressed genes. Gene response of the two host lines strongly differed depending on the sugar level. Limited colonization of HighSC line by C. gloeosporioides was accompanied by a marked alteration of gene expression compared the LowSC response to the same pathogen; while colonization by P. expansum resulted in a similar response of the two different hosts. We suggest that this differential pattern of fungal/host responses may be the basis for the differential of host range of both pathogens in nature.

Note:
Related Files :
Colletotrichum
Colletotrichum gloeosporioides
Pathogens
Penicillium
Penicillium expansum
Postharvest diseases
Tomato fruit
עוד תגיות
תוכן קשור
More details
DOI :
10.1111/1462-2920.15031
Article number:
0
Affiliations:
Database:
גוגל סקולר
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
47431
Last updated date:
02/03/2022 17:27
Creation date:
29/04/2020 02:01
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Scientific Publication
Sugar‐regulated susceptibility of tomato fruit to Colletotrichum and Penicillium requires differential mechanisms of pathogenicity and fruit responses

Maxim Itkin - Life Science Core Facilities, Weizmann Institute of Science, Rehovot, 7610001 Israel.
Sergey Malitsky - Life Science Core Facilities, Weizmann Institute of Science, Rehovot, 7610001 Israel
 

Sugar‐regulated susceptibility of tomato fruit to Colletotrichum and Penicillium requires differential mechanisms of pathogenicity and fruit responses

Colletotrichum gloeosporioides and Penicillium expansum cause postharvest diseases in tropical and deciduous fruit. During colonization, C. gloeosporioides and P. expansum secrete ammonia in hosts with low sugar content (LowSC) and gluconic acid in hosts with high sugar content (HighSC), respectively, as a mechanism to modulate enhanced pathogenicity. We studied the pathogens interactions with tomato lines of similar genetic background but differing in their sugar content. C. gloeosporioides showed enhanced colonization of the LowSC line with differential expression response of 15% of its genes including enhanced relative expression of glycosyl hydrolases, glucanase and MFS‐transporter genes. Enhanced colonization of P. expansum occurred in the HighSC line, accompanied by an increase in carbohydrate metabolic processes mainly phosphoenolpyruvate carboxykinase, and only 4% of differentially expressed genes. Gene response of the two host lines strongly differed depending on the sugar level. Limited colonization of HighSC line by C. gloeosporioides was accompanied by a marked alteration of gene expression compared the LowSC response to the same pathogen; while colonization by P. expansum resulted in a similar response of the two different hosts. We suggest that this differential pattern of fungal/host responses may be the basis for the differential of host range of both pathogens in nature.

Scientific Publication
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