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(2) Signal distribution through the potato tissues.
Thus, sterol deficiency in the AA-immunized potato tissues can be one of the defense reactions to infection caused by P. infestans[29].
Electron-microscopic examinations revealed considerable changes in ultrastructure of AA-treated potato tissues: an increase both in the volume of agranular reticulum and in the number of mitochondria [29].
High concentrations of the AA preparation (5 10−5 M and higher) induced necrosis of potato tissues and synthesis of phytoalexins (PA), which were accumulated in necrotizing tissues in toxic for pathogen concentrations showing defense effect on plant.
It is known that sterols play important role in the interactions of P. infestans with potato tissues, since the fungus exhibits auxotrophic requirements for sterols and fill up sterol deficiency at the expense of the host tissues [29].
(3) Period of reorganization of metabolism and structure of potato tissues (usually from 48 to 96 h), which includes considerable changes in cell ultrastructure, an increase in the amounts of enzymes and protective substances, and a decrease in sterol content.
Similar(43)
Heat transfer coefficient of the steam peeler and thermal diffusivity of the potato tissue were experimentally obtained.
Y2H screens were performed on a mixed potato tissue cDNA library described in [ 19], following standard procedures as previously described in [ 20].
Suzuki et al. [ 34] correlated a transient induction of HMGR activity with the accumulation of ipomeamarone, a furanosesquiterpenoid, in sweet potato tissue infected with Ceratocystis fimbriata.
High levels of initial attachment have been noted for other organisms with rapid attachment within 1 min recorded for Campylobacter on stainless steel [ 20] and Listeria and Pseudomonas on raw potato tissue [ 21].
Total RNA was prepared from sweet potato leaf tissues using the pine tree method.
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