Details
| Original language | English |
|---|---|
| Qualification | Doctor rerum horticulturarum |
| Awarding Institution | |
| Supervised by |
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| Date of Award | 10 Jul 2024 |
| Place of Publication | Hannover |
| Publication status | Published - 16 Jul 2024 |
Abstract
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Hannover, 2024. 177 p.
Research output: Thesis › Doctoral thesis
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TY - BOOK
T1 - The impaired barrier function of the cuticle triggers russeting
AU - Chen, Yun-Hao
PY - 2024/7/16
Y1 - 2024/7/16
N2 - Russeting is a physiological disorder that occurs in several economically important crops. Among these, apple is a prominent case. Previous studies on the etiology of russeting in apple indicate that (1) moisture and wounding are common inducers of russeting; (2) russeting is associated with cuticular microcracking; and (3) the early stage of fruit development is more susceptible to russeting than the later stages. However, the initial events of russeting remain unknown. To elucidate the etiology of russeting, the objectives of the present study were to investigate: (1) the effect of prolonged surface moisture on apple fruit; (2) the sequence of events during exposure to surface moisture and after its removal; (3) the similarity between the events caused by wounding and moisture and their resulting periderm; (4) the initial processes of russeting using a transcriptomic approach; (5) the potential role of atmospheric oxygen (O2) in russeting. Exposure of young apple fruit to surface moisture for 12 days (d) induced microcracking, increased water loss, and led to russeting. Using the same exposure technique, moisture- induced periderm was found to be biphasic: a periderm initiated only after moisture removal (Phase II) and required at least 6 d of exposure (Phase I) to change cuticle properties to form an impaired barrier and induce russeting. The moisture-induced and wound periderm shared similarities in their initiation at the histological level, the initial expression pattern of several lignin, suberin, cutin and wax-related genes and the chemical constituents at fruit maturity. Additional phase-specific expression profiles of the moisture-induced periderm are revealed by transcriptome. Further efforts were made to establish detached fruit systems in young apple and tomato fruit to study the role of O2 in russeting under anoxia. Unfortunately, the apple system failed due to various problems, but a promising tomato system, which behaved similarly to the attached fruit was later used for this purpose. The exclusion of O2 successfully prevented the formation of a wound periderm. This was demonstrated by the absence of a periderm after 8 d of wounding and the suppression of selected suberin and lignin-related genes. In conclusion, the results of the present study provide evidence that an impaired barrier caused by microcracking triggers the process of russeting. This triggering is O2-dependent.
AB - Russeting is a physiological disorder that occurs in several economically important crops. Among these, apple is a prominent case. Previous studies on the etiology of russeting in apple indicate that (1) moisture and wounding are common inducers of russeting; (2) russeting is associated with cuticular microcracking; and (3) the early stage of fruit development is more susceptible to russeting than the later stages. However, the initial events of russeting remain unknown. To elucidate the etiology of russeting, the objectives of the present study were to investigate: (1) the effect of prolonged surface moisture on apple fruit; (2) the sequence of events during exposure to surface moisture and after its removal; (3) the similarity between the events caused by wounding and moisture and their resulting periderm; (4) the initial processes of russeting using a transcriptomic approach; (5) the potential role of atmospheric oxygen (O2) in russeting. Exposure of young apple fruit to surface moisture for 12 days (d) induced microcracking, increased water loss, and led to russeting. Using the same exposure technique, moisture- induced periderm was found to be biphasic: a periderm initiated only after moisture removal (Phase II) and required at least 6 d of exposure (Phase I) to change cuticle properties to form an impaired barrier and induce russeting. The moisture-induced and wound periderm shared similarities in their initiation at the histological level, the initial expression pattern of several lignin, suberin, cutin and wax-related genes and the chemical constituents at fruit maturity. Additional phase-specific expression profiles of the moisture-induced periderm are revealed by transcriptome. Further efforts were made to establish detached fruit systems in young apple and tomato fruit to study the role of O2 in russeting under anoxia. Unfortunately, the apple system failed due to various problems, but a promising tomato system, which behaved similarly to the attached fruit was later used for this purpose. The exclusion of O2 successfully prevented the formation of a wound periderm. This was demonstrated by the absence of a periderm after 8 d of wounding and the suppression of selected suberin and lignin-related genes. In conclusion, the results of the present study provide evidence that an impaired barrier caused by microcracking triggers the process of russeting. This triggering is O2-dependent.
U2 - 10.15488/17786
DO - 10.15488/17786
M3 - Doctoral thesis
CY - Hannover
ER -