نظام إشارات الميتوكوندريا

One of the central problems of modern phytobiology is the study of the mechanisms of genetic determination of plant resistance to adverse environmental factors, among which
temperature plays a special role. Indeed, changes in external conditions, including the effect
of stressful temperature factors, cause
significant changes in the metabolism of plant cells. At the same time, a program of selective gene expression is being implemented and
mechanisms of genetic determination of plant resistance to stress are being implemented.
Such a program is carried out in the whole cell system and includes many
stages: reception of a signal about the action of a stress factor, signal transduction into the cell and
into the genome, changes in the expression of a number of genes,
synthesis of proteins (stress proteins) with specific functions, the functioning of these
proteins, changes in cell metabolism. These stages proceed in concert, i.e. there
is intracellular integration aimed at
the formation of cell resistance to stress.
All these stages are of considerable
interest, but in this paper we will only talk about
on the interaction of information and energy systems of a cell under stress: on the expression of stress proteins, on their functions, on
nuclear-mitochondrial relationships
during redox regulation of gene
expression during low-temperature stress.
Material and methods
Seedlings and adult plants of winter wheat (Triticum aestivum L.) and rye (Secale cereale L.), corn (
Zea mays L.), yeast (Saccharomyces cerevisiae),
suspension and callus culture of Arabidopsis cells
(Arabidopsis thaliana) were used in the work. Temperature treatment of the material used in the work
the material was carried out as described earlier [6; 7;
10; 11; 12]. All temperature treatment of plant material was carried out under controlled climate conditions in the climatic chambers of the phytotron. The previously
described techniques were used for: isolation of mitochondria [1], for the analysis of free fatty acids [12], for the isolation and study of the composition
of stress proteins [8; 9].
Results and discussion
It was previously shown that with
temperature fluctuations, strong changes occur in
the energy activity of mitochondria and these
changes are genetically determined [2].
Temperature fluctuations lead to changes in the composition of lipids of mitochondrial membranes and in the amount and degree of saturation
of free fatty acids [12]. Probably, these
events can be considered as a signal about
the effect of stress. An increase in the amount of free fatty acids leads to a change
noy membrane. The mechanism of the uncoupling action of free fatty acids was determined [5] and the role of the uncoupling PUMP protein and ADP/ATP antiporter in this process was determined. Coordination of the work of respiratory chain complexes and systems separating
oxidative phosphorylation is shown [9].
With hypothermia, classical uncoupling proteins, free fatty acids and a non-specific pore begin to work. All this
leads to a decrease in the conjugacy of oxidative phosphorylation, to a decrease
in the level of free oxygen forms and to local thermogenesis in cells [5]. It is shown that
thermogenesis, as a mechanism of protection against low-temperature stress, is widespread in
the plant kingdom and is one of the ways to protect plants that are not adapted to
low temperature from damage.
With temperature fluctuations, the synthesis of stress proteins occurs simultaneously with changes in mitochondrial activity. For example, when plants are cooled, many stress proteins are synthesized (Fig. 1).
Fig. 1. Stress proteins of tillering nodes of winter
wheat. The dates of sampling of the season are indicated above
2001-2002
Differential expression is shown
stress genes. It was found that the expression
these genes depend on the type of stress. At the same
time, there are genes that are expressed
under any stress [3].
It turned out that mitochondria
are involved in regulating the activity of a number of stress genes. For example, the dependence
of the expression of stress protein genes on the redox state of the respiratory chain
of yeast mitochondria has been established. It has been shown that during heat shock
, hyperpolarization of the inner mitochondrial membrane occurs, induction of gene expression of heat shock proteins and an increase
in cell resistance to hyperthermia.
Elimination of hyperpolarization of the membrane with
the help of oxidative phosphorylation disconnectors or protonophores leads to
the termination of the expression of the HSP 104 gene and to the loss of resistance to temperature by cells [10]. Consequently, the redox state
of the inner mitochondrial membrane regulates the expression of genes of thermal protein
It determines the level of thermal tolerance of cells (Fig. 2).
Fig. 2. Redox regulation of the expression of heat shock genes
Using suspension cells and
tissue cultures of arabidopsis transgenic lines with semantic and antisense sequences of the HSP 101 stress protein gene
(plant analogue of the protein HSP 104) the dependence of the thermal stability of plant
cells on the synthesis of this protein is shown [11]. Thus, during temperature fluctuations in
plant cells, a signaling system associated with mitochondria functions (Fig. 3). This system perceives the onset of temperature stress, transmits a signal about it to the genome and
changes the expression of the corresponding genes controlling the synthesis of stress proteins