Details
| Original language | English |
|---|---|
| Pages (from-to) | 653-660 |
| Number of pages | 8 |
| Journal | Journal of the American Society for Horticultural Science |
| Volume | 141 |
| Issue number | 6 |
| Publication status | Published - 1 Nov 2016 |
Abstract
Rain cracking of sweet cherry (Prunus avium L.) fruit is commonly thought to result from excessive net water uptake. This excess increases flesh turgor, which then strains and eventually ruptures the skin at the weakest point. This idea—the critical turgor hypothesis—assumes the fruit comprises a semifluid flesh, held under pressure by a taut skin. The objectives of this study were to test the validity of this popular hypothesis. We investigated the effects of 1) the different pathways of water uptake and 2) the fruit’s water balance on cracking. Incubating fruit of 19 cultivars in water resulted in rapid fruit cracking. The time to 50% cracking (T50) averaged 7.5 ± 1.3 hours with considerable variability between cultivars (T50 range from 1.5 to 18.6 hours). The amount of water taken up at 50% cracking (WU50) averaged 96.5 ± 17.6 mg (WU50 range from 17.7 to 331.5 mg). There was no correlation between either the T50 or the WU50, and the rate of water uptake. Also, there was no correlation between the values of T50 (r = 0.58) and only a weak correlation between the values of WU50 (r = 0.80*) determined in different years. Comparing the value of WU50 under incubation vs. under perfusion revealed a 3.9-to 38-fold higher WU50 under perfusion (397.6 to 1840 mg) than under incubation (48.8 to 102.6 mg). This marked dissimilarity remained, regardless of pretreatments with isotonic polyethylene glycol (PEG) 6000 to induce microcracking or by manipulation of skin wetness during perfusion. Sealing the pedicel/fruit junction markedly decreased the rate of water uptake under incubation. It had no effect on the T50, and it markedly decreased the WU50. Similarly, manually induced skin defects greatly increased the rate of water uptake but, with few exceptions, had no effect on the T50, whereas, theWU50 had increased. The location on the fruit surface of the resulting cracks was not related to the region of the skin in which the manual defect was induced. Allowing the fruit to transpire increased both, the T50 and theWU50. Interestingly, the amount of water lost by transpiration exceeded the amount that was subsequently required to cause cracking up to 5-fold. Incubating fruit with their stylar ends immersed in water, whereas their remaining surfaces were in air of 0%, 28%, 75%, or 100% relative humidity (RH) resulted in net losses of water of up to 5.9 ± 0.7 mg·h-1, nevertheless their stylar ends still cracked. All our results indicate rain cracking in sweet cherries is a localized phenomenon that is not related to the net fruit water balance (the critical turgor hypothesis) but is the result of more local exposure of the fruit skin to liquid-phase water (the zipper hypothesis).
Keywords
- Perfusor, Prunus avium, Splitting, Strain, Turgor
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Genetics
- Agricultural and Biological Sciences(all)
- Horticulture
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In: Journal of the American Society for Horticultural Science, Vol. 141, No. 6, 01.11.2016, p. 653-660.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Rain cracking in sweet cherries is not due to excess water uptake but to localized skin phenomena
AU - Winkler, Andreas
AU - Peschel, Stefanie
AU - Kohrs, Kathleen
AU - Knoche, Moritz
N1 - Funding Information: This research was funded in part by a grant from the DFGDeutsche Forschungsgemeinschaft.
PY - 2016/11/1
Y1 - 2016/11/1
N2 - Rain cracking of sweet cherry (Prunus avium L.) fruit is commonly thought to result from excessive net water uptake. This excess increases flesh turgor, which then strains and eventually ruptures the skin at the weakest point. This idea—the critical turgor hypothesis—assumes the fruit comprises a semifluid flesh, held under pressure by a taut skin. The objectives of this study were to test the validity of this popular hypothesis. We investigated the effects of 1) the different pathways of water uptake and 2) the fruit’s water balance on cracking. Incubating fruit of 19 cultivars in water resulted in rapid fruit cracking. The time to 50% cracking (T50) averaged 7.5 ± 1.3 hours with considerable variability between cultivars (T50 range from 1.5 to 18.6 hours). The amount of water taken up at 50% cracking (WU50) averaged 96.5 ± 17.6 mg (WU50 range from 17.7 to 331.5 mg). There was no correlation between either the T50 or the WU50, and the rate of water uptake. Also, there was no correlation between the values of T50 (r = 0.58) and only a weak correlation between the values of WU50 (r = 0.80*) determined in different years. Comparing the value of WU50 under incubation vs. under perfusion revealed a 3.9-to 38-fold higher WU50 under perfusion (397.6 to 1840 mg) than under incubation (48.8 to 102.6 mg). This marked dissimilarity remained, regardless of pretreatments with isotonic polyethylene glycol (PEG) 6000 to induce microcracking or by manipulation of skin wetness during perfusion. Sealing the pedicel/fruit junction markedly decreased the rate of water uptake under incubation. It had no effect on the T50, and it markedly decreased the WU50. Similarly, manually induced skin defects greatly increased the rate of water uptake but, with few exceptions, had no effect on the T50, whereas, theWU50 had increased. The location on the fruit surface of the resulting cracks was not related to the region of the skin in which the manual defect was induced. Allowing the fruit to transpire increased both, the T50 and theWU50. Interestingly, the amount of water lost by transpiration exceeded the amount that was subsequently required to cause cracking up to 5-fold. Incubating fruit with their stylar ends immersed in water, whereas their remaining surfaces were in air of 0%, 28%, 75%, or 100% relative humidity (RH) resulted in net losses of water of up to 5.9 ± 0.7 mg·h-1, nevertheless their stylar ends still cracked. All our results indicate rain cracking in sweet cherries is a localized phenomenon that is not related to the net fruit water balance (the critical turgor hypothesis) but is the result of more local exposure of the fruit skin to liquid-phase water (the zipper hypothesis).
AB - Rain cracking of sweet cherry (Prunus avium L.) fruit is commonly thought to result from excessive net water uptake. This excess increases flesh turgor, which then strains and eventually ruptures the skin at the weakest point. This idea—the critical turgor hypothesis—assumes the fruit comprises a semifluid flesh, held under pressure by a taut skin. The objectives of this study were to test the validity of this popular hypothesis. We investigated the effects of 1) the different pathways of water uptake and 2) the fruit’s water balance on cracking. Incubating fruit of 19 cultivars in water resulted in rapid fruit cracking. The time to 50% cracking (T50) averaged 7.5 ± 1.3 hours with considerable variability between cultivars (T50 range from 1.5 to 18.6 hours). The amount of water taken up at 50% cracking (WU50) averaged 96.5 ± 17.6 mg (WU50 range from 17.7 to 331.5 mg). There was no correlation between either the T50 or the WU50, and the rate of water uptake. Also, there was no correlation between the values of T50 (r = 0.58) and only a weak correlation between the values of WU50 (r = 0.80*) determined in different years. Comparing the value of WU50 under incubation vs. under perfusion revealed a 3.9-to 38-fold higher WU50 under perfusion (397.6 to 1840 mg) than under incubation (48.8 to 102.6 mg). This marked dissimilarity remained, regardless of pretreatments with isotonic polyethylene glycol (PEG) 6000 to induce microcracking or by manipulation of skin wetness during perfusion. Sealing the pedicel/fruit junction markedly decreased the rate of water uptake under incubation. It had no effect on the T50, and it markedly decreased the WU50. Similarly, manually induced skin defects greatly increased the rate of water uptake but, with few exceptions, had no effect on the T50, whereas, theWU50 had increased. The location on the fruit surface of the resulting cracks was not related to the region of the skin in which the manual defect was induced. Allowing the fruit to transpire increased both, the T50 and theWU50. Interestingly, the amount of water lost by transpiration exceeded the amount that was subsequently required to cause cracking up to 5-fold. Incubating fruit with their stylar ends immersed in water, whereas their remaining surfaces were in air of 0%, 28%, 75%, or 100% relative humidity (RH) resulted in net losses of water of up to 5.9 ± 0.7 mg·h-1, nevertheless their stylar ends still cracked. All our results indicate rain cracking in sweet cherries is a localized phenomenon that is not related to the net fruit water balance (the critical turgor hypothesis) but is the result of more local exposure of the fruit skin to liquid-phase water (the zipper hypothesis).
KW - Perfusor
KW - Prunus avium
KW - Splitting
KW - Strain
KW - Turgor
UR - http://www.scopus.com/inward/record.url?scp=85007579945&partnerID=8YFLogxK
U2 - 10.21273/JASHS03937-16
DO - 10.21273/JASHS03937-16
M3 - Article
AN - SCOPUS:85007579945
VL - 141
SP - 653
EP - 660
JO - Journal of the American Society for Horticultural Science
JF - Journal of the American Society for Horticultural Science
SN - 0003-1062
IS - 6
ER -