scholarly journals The wound hormone jasmonate

2009 ◽  
Vol 70 (13-14) ◽  
pp. 1571-1580 ◽  
Author(s):  
Abraham J.K. Koo ◽  
Gregg A. Howe
Keyword(s):  
2017 ◽  
Vol 218 (3) ◽  
pp. 1167-1178 ◽  
Author(s):  
Roman E. Beloshistov ◽  
Konrad Dreizler ◽  
Raisa A. Galiullina ◽  
Alexander I. Tuzhikov ◽  
Marina V. Serebryakova ◽  
...  

ChemInform ◽  
2010 ◽  
Vol 41 (7) ◽  
Author(s):  
Abraham J. K. Koo ◽  
Gregg A. Howe
Keyword(s):  

Science ◽  
1937 ◽  
Vol 86 (2233) ◽  
pp. 352-353 ◽  
Author(s):  
J. Bonner ◽  
J. English
Keyword(s):  

A study has been made of the abnormally high mitotic activity seen in mouse epidermis adjacent to a wound. Such activity is in the form of a gradient, no more than about 1 mm long, with the highest mitotic rate adjacent to the cut edge. It is shown that this gradient is not due to differential damage or to the effects of local hyperaemia. When the hypodermis and dermis are wounded from below, the overlying undamaged epidermis does not react by mitosis. Such a wound includes damage to the panniculus carnosus, the hair follicles and the sebaceous glands. It also involves hyperaemia and an invasion of leucocytes. It therefore appears that damage to the epidermis itself is necessary before an epidermal reaction can develop. Such a reaction could be due either to the secretion by the damaged epidermis of a mitosis stimulating ‘wound hormone' or to the local elimination of a normally present epidermal mitotic inhibitor. It was observed that when one side of the ear is wounded high mitotic activity develops in the opposite undamaged epidermis, which is less than 1 mm distant. In further experiments it was found that the greatest reaction in a sheet of undamaged ear epidermis is opposite the centre of an area from which the epidermis has been removed altogether. Since the area from which the epidermis was removed was 3 mm square, it is obvious that an epidermal ‘wound hormone' could not have been present in effective concentration in the central region, but the absence of an inhibitor which would normally have been present could explain the result obtained. It is therefore concluded that the gradient of epidermal mitotic activity adjacent to a wound may be inversely proportional to a gradient of mitotic inhibitor, which may cease to be produced within damaged cells and which may also diffuse away into the cavity of a wound. The question of the possible presence within the adult mouse of a complex of growth-controlling tissue-specific inhibitors is discussed, and evidence for its existence is reviewed.


1938 ◽  
Vol 13 (2) ◽  
pp. 331-348 ◽  
Author(s):  
James Bonner ◽  
James English

2004 ◽  
Vol 94 (11) ◽  
pp. 1207-1214 ◽  
Author(s):  
I. R. Soriano ◽  
R. E. Asenstorfer ◽  
O. Schmidt ◽  
I. T. Riley

The induction of defense compounds in oats (Avena sativa) in response to invasion by parasitic nematodes and to application of the wound hormone methyl jasmonate was examined. Oats cv. Quoll seedlings were challenged with Pratylenchus neglectus, Heterodera avenae, and Ditylenchus dipsaci and treated with 1 × 10-4 M methyl jasmonate. Three compounds, isolated in methanolic root and shoot extracts of oats, exhibiting an absorbance spectrum typical of flavone glycosides, were induced by nematode invasion and methyl jasmonate. These were identified as flavone-C-glycosides by mass spectrometry. The effect of the flavone-C-glycosides on the invasion by and development of cereal cyst nematode H. avenae was assessed using methanolic extracts of shoots and roots from methyl jasmonate-treated plants. Both extracts impaired nematode invasion and development. When the extracts were fractionated by high voltage paper electrophoresis, only one flavone-C-glycoside, O-methyl-apigenin-C-deoxyhexoside-O-hexoside, inhibited nematode invasion. The protective effect of the induction of flavone-C-glycosides in oats by methyl jasmonate was evaluated against H. avenae and P. neglectus. Treatment with methyl jasmonate reduced invasion of both nematodes and increased plant mass, compensating for damage caused by the nematodes, and is attributed to the active flavone-C-glycoside. The active compound, O-methyl-apigenin-C-deoxyhexoside-O-hexoside, has not been implicated previously in plant defense against any pest or pathogen, and appears to provide protection against the major cereal nematodes Heterodera and Pratylenchus.


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