TY - JOUR

T1 - Crack initiation and propagation in sweet cherry skin: A simple chain reaction causes the crack to ‘run’

AU - Schumann, Christine

AU - Winkler, Andreas

AU - Brüggenwirth, Martin

AU - Köpcke, Kevin

AU - Knoche, Moritz

N1 - Funding information: This study was funded in part by a grant from the DFG (KN 402) to M.K. and from the Gisela Foundation to A.W. The publication of this article was funded by the Open Access fund of Leibniz Universität Hannover. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank Dr. Paul Knox, University of Leeds, UK for useful comments on technical aspects of immunolabeling of cell walls in fleshy fruit and the generous gift of the antibodies LM7, LM11, LM15, LM21 and LM25 and Dr. Alexander Lang for helpful comments on an earlier version of this manuscript.

PY - 2019/7/31

Y1 - 2019/7/31

N2 - Rain cracking severely affects the commercial production of many fleshy-fruit species, including of sweet cherries. The objectives were to investigate how the gaping macroscopic cracks (macrocracks) of a rain-cracked fruit can develop from microscopic cracks in the cuticle (microcracks). Incubating fruit in deionized water is well known to cause significant macrocracking. We found that after a lag phase of 2 h, the numbers and lengths of macrocracks increased. Macrocrack number approached an asymptote at 12 h, whereas macrocrack length continued to increase. The rate of macrocrack propagation (extension at the crack tip) was initially 10.8 mm h-1 but then decreased to a near-constant 0.5 mm h-1. Light microscopy revealed three characteristic zones along a developing macrocrack. In zone I (ahead of the crack), the cuticle was intact, the epidermal cells were unbroken and their cell walls were thin. In zone II, the cuticle was fractured, the first epidermal cells died and their cell walls began to thicken (swell). In zone III, most epidermal cells had died, their cell walls were swollen and cell:cell separation began along the middle lamellae. The thickness of the anticlinal epidermal cell walls and the percentage of intact living cells along a crack were closely and negatively related. Cracks were stained by calcofluor white, but there was no binding of monoclonal antibodies (mAbs) specific for hemicelluloses (LM11, LM21, LM25). Strong binding was obtained with the anti-homogalacturonan mAb (LM19), indicating the presence of unesterified homogalacturonans on the crack surface. We conclude that macrocrack propagation is related to cell death and to cell wall swelling. Cell wall swelling weakens the cell:cell adhesion between neighbouring epidermal cells, which separate along their middle lamellae. The skin macrocrack propagates like a ‘run’ in a fine, knitted fabric.

AB - Rain cracking severely affects the commercial production of many fleshy-fruit species, including of sweet cherries. The objectives were to investigate how the gaping macroscopic cracks (macrocracks) of a rain-cracked fruit can develop from microscopic cracks in the cuticle (microcracks). Incubating fruit in deionized water is well known to cause significant macrocracking. We found that after a lag phase of 2 h, the numbers and lengths of macrocracks increased. Macrocrack number approached an asymptote at 12 h, whereas macrocrack length continued to increase. The rate of macrocrack propagation (extension at the crack tip) was initially 10.8 mm h-1 but then decreased to a near-constant 0.5 mm h-1. Light microscopy revealed three characteristic zones along a developing macrocrack. In zone I (ahead of the crack), the cuticle was intact, the epidermal cells were unbroken and their cell walls were thin. In zone II, the cuticle was fractured, the first epidermal cells died and their cell walls began to thicken (swell). In zone III, most epidermal cells had died, their cell walls were swollen and cell:cell separation began along the middle lamellae. The thickness of the anticlinal epidermal cell walls and the percentage of intact living cells along a crack were closely and negatively related. Cracks were stained by calcofluor white, but there was no binding of monoclonal antibodies (mAbs) specific for hemicelluloses (LM11, LM21, LM25). Strong binding was obtained with the anti-homogalacturonan mAb (LM19), indicating the presence of unesterified homogalacturonans on the crack surface. We conclude that macrocrack propagation is related to cell death and to cell wall swelling. Cell wall swelling weakens the cell:cell adhesion between neighbouring epidermal cells, which separate along their middle lamellae. The skin macrocrack propagates like a ‘run’ in a fine, knitted fabric.

UR - http://www.scopus.com/inward/record.url?scp=85070062061&partnerID=8YFLogxK

U2 - 10.1371/journal.pone.0219794

DO - 10.1371/journal.pone.0219794

M3 - Article

C2 - 31365556

AN - SCOPUS:85070062061

VL - 14

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 7

M1 - e0219794

ER -