The ultrastructure of chilling stress
Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum...
Ausführliche Beschreibung
Autor*in: |
Kratsch, H. A. [verfasserIn] Wise, R. R. [verfasserIn] |
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E-Artikel |
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Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2000 |
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Online-Ressource |
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Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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Übergeordnetes Werk: |
In: Plant, cell & environment - Oxford [u.a.] : Wiley-Blackwell, 1978, 23(2000), 4, Seite 0 |
Übergeordnetes Werk: |
volume:23 ; year:2000 ; number:4 ; pages:0 |
Links: |
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DOI / URN: |
10.1046/j.1365-3040.2000.00560.x |
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520 | |a Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. | ||
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10.1046/j.1365-3040.2000.00560.x doi (DE-627)NLEJ243844689 DE-627 ger DE-627 rakwb Kratsch, H. A. verfasserin aut The ultrastructure of chilling stress Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| chilling stress Wise, R. R. verfasserin aut In Plant, cell & environment Oxford [u.a.] : Wiley-Blackwell, 1978 23(2000), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926944 (DE-600)2020843-1 1365-3040 nnns volume:23 year:2000 number:4 pages:0 http://dx.doi.org/10.1046/j.1365-3040.2000.00560.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 2000 4 0 |
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10.1046/j.1365-3040.2000.00560.x doi (DE-627)NLEJ243844689 DE-627 ger DE-627 rakwb Kratsch, H. A. verfasserin aut The ultrastructure of chilling stress Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| chilling stress Wise, R. R. verfasserin aut In Plant, cell & environment Oxford [u.a.] : Wiley-Blackwell, 1978 23(2000), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926944 (DE-600)2020843-1 1365-3040 nnns volume:23 year:2000 number:4 pages:0 http://dx.doi.org/10.1046/j.1365-3040.2000.00560.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 2000 4 0 |
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10.1046/j.1365-3040.2000.00560.x doi (DE-627)NLEJ243844689 DE-627 ger DE-627 rakwb Kratsch, H. A. verfasserin aut The ultrastructure of chilling stress Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| chilling stress Wise, R. R. verfasserin aut In Plant, cell & environment Oxford [u.a.] : Wiley-Blackwell, 1978 23(2000), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926944 (DE-600)2020843-1 1365-3040 nnns volume:23 year:2000 number:4 pages:0 http://dx.doi.org/10.1046/j.1365-3040.2000.00560.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 2000 4 0 |
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10.1046/j.1365-3040.2000.00560.x doi (DE-627)NLEJ243844689 DE-627 ger DE-627 rakwb Kratsch, H. A. verfasserin aut The ultrastructure of chilling stress Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| chilling stress Wise, R. R. verfasserin aut In Plant, cell & environment Oxford [u.a.] : Wiley-Blackwell, 1978 23(2000), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926944 (DE-600)2020843-1 1365-3040 nnns volume:23 year:2000 number:4 pages:0 http://dx.doi.org/10.1046/j.1365-3040.2000.00560.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 2000 4 0 |
allfieldsSound |
10.1046/j.1365-3040.2000.00560.x doi (DE-627)NLEJ243844689 DE-627 ger DE-627 rakwb Kratsch, H. A. verfasserin aut The ultrastructure of chilling stress Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| chilling stress Wise, R. R. verfasserin aut In Plant, cell & environment Oxford [u.a.] : Wiley-Blackwell, 1978 23(2000), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926944 (DE-600)2020843-1 1365-3040 nnns volume:23 year:2000 number:4 pages:0 http://dx.doi.org/10.1046/j.1365-3040.2000.00560.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 2000 4 0 |
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Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. |
abstractGer |
Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. |
abstract_unstemmed |
Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ243844689</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707190442.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2000 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.1365-3040.2000.00560.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ243844689</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Kratsch, H. A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">The ultrastructure of chilling stress</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science Ltd</subfield><subfield code="c">2000</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Chilling injury to crop plants was first described 70 years ago and has been systematically investigated with electron microscopy since the late 1960s. Chloroplasts are the first and most severely impacted organelle. Thylakoids swell and distort, starch granules disappear, and a peripheral reticulum (vesicles arising from inner membrane of chloroplast envelope) appears. Chloroplast disintegration follows prolonged chilling. Mitochondria, nuclei and other organelles are less susceptible to chilling injury. Organellar development and ontogeny may also be disrupted. The inherent chilling sensitivity of a plant, as well as the ability of some species to acclimate to chilling, influence the timing and appearance of ultrastructural injury with the resulting outcome being mild, moderate, or severe. Other environmental factors that exacerbate injury are irradiance, chilling duration, and water status. The physiological basis for chloroplast swelling may be linked to chilling-stable starch-degrading enzymes that produce soluble sugars thus lowering stromal water potential at a time when chloroplast photosynthate export is reduced. Thylakoid dilation appears to be related to photo-oxidative conditions produced during chilling in the light. The peripheral reticulum is proposed to increase surface area of the transport-limiting membrane (chloroplast inner membrane) in response to the chilling-induced reduction in metabolite transport. Many of the ultrastructural symptoms appearing during moderate stress resemble those seen in programmed cell death. Future research directions are discussed.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2001</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2001||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">chilling stress</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wise, R. R.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Plant, cell & environment</subfield><subfield code="d">Oxford [u.a.] : Wiley-Blackwell, 1978</subfield><subfield code="g">23(2000), 4, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926944</subfield><subfield code="w">(DE-600)2020843-1</subfield><subfield code="x">1365-3040</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:23</subfield><subfield code="g">year:2000</subfield><subfield code="g">number:4</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.1365-3040.2000.00560.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">23</subfield><subfield code="j">2000</subfield><subfield code="e">4</subfield><subfield code="h">0</subfield></datafield></record></collection>
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