THE EFFECT OF ABA AND IAA PHYTOHORMONES ON THE REDUCING SUGARS AND ENDOGENOUS PHYTOHORMONES CONTENT OF COTTON PLANT UNDER SALIFICATION

Author(s):  
K. M. Kuldoshova ◽  
А. А. Akhunov ◽  
N. R. Khashimova ◽  
D. T. Babaeva ◽  
М. I. Nurmatova

This article investigates the effect of exogenous phytohormones ABA and IAA on the content of reducing sugars and endogenous phytohormones in cotton seedlings of varieties Porlok-4, obtained on the basis of gene knockout technology and a marker of associated breeding - Ravnak-1. Exogenous phytohormones (ABA and IAA) can significantly change the level of cotton resistance to unfavorable environmental factors. Under the action of exogenous ABA causes an increase of cotton resistance to salinity. Biotechnological cotton variety Ravnak-1 showed sensitivity to prolonged exposure to salinity in combination with phytohormones, increasing the content of reducing sugars and endogenous phytohormones, depending on the duration of salt stress. In the Porlok-4 variety, under the influence of salinity, the content of reducing sugars and endogenous phytohormones had an insignificant increase, due to the inherent adaptive capacity of the variety. The conducted studies allow us to conclude that phytohormones are actively involved in the formation of cotton resistance to the action of unfavorable environmental factors of an abiotic nature.

2007 ◽  
Vol 20 (2) ◽  
Author(s):  
Hao-Chih Tai ◽  
Mohamed Ezzelarab ◽  
Hidetaka Hara ◽  
David Ayares ◽  
David K.C. Cooper

1997 ◽  
Vol 3 (S2) ◽  
pp. 317-318
Author(s):  
David A. Sanan ◽  
Dale L. Newland

Build-up of visible atherosclerotic plaque in the arteries is readily quantifiable. The mouse and the rabbit provide useful models for understanding the pathogenesis of atherosclerosis by investigating the effects of genetic and dietary perturbations.Although the wild type mouse does not develop atherosclerosis, atherosclerosis susceptibility genes have been identified in some laboratory mouse strains which do. Furthermore, transgenic technology and gene targeting have produced genetically modified mice that express various apolipoproteins, enzymes and cofactors involved in human lipoprotein metabolism. Gene “knockout” technology allows transgene expression without interference from homologous genes. One notable “knockout” mouse, deficient in apolipoprotein E, develops spontaneous atherosclerosis on a normal chow diet. Transgenic modulations of the atherosclerotic responses of these highly susceptible mice are more pronounced and easily measured. Small, cheap and fast breeding, mice are convenient animal models. But to make mice susceptible to atherosclerosis, their genetic background has to be so drastically altered that the resulting lipoprotein metabolism may not model the human metabolism accurately enough.


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