TRANSCRIPTION FACTOR BINDING SITES IN A STRUCTURAL GENE: WHAT MAY BE THIS? (BY THE EXAMPLE OF THE GENES ENCODING THE MAIN ENZYMES OF THE POLYAMINES METABOLISM) Текст научной статьи по специальности «Биологические науки»

TRANSCRIPTION FACTOR BINDING SITES IN A STRUCTURAL GENE: WHAT MAY BE THIS? (BY THE EXAMPLE OF THE GENES ENCODING THE MAIN ENZYMES OF THE

POLYAMINES METABOLISM)

O.A.Orlovsky

Ph.D (Biol), D.Sc(MA), staff scientist, R.E.Kavetsky Institute of experimental pathology, oncology and radiobiology

NAS of Ukraine, Kyiv O.A.Samoylenko Principal engineer, the same place of employment V.O. Shlyakhovenko

Doctor of medicine, professor, principal staff scientist, the same place of employment

This paper is an attempt to elucidate one question - quite simple but have been never put directly in any contemporary publication we know: what may be function of the transcription factors binding sites (TFBS) located not in the promoters but in the structural genes. Human and mouse genes (both structural genes and their promoters) encoding 6 main enzymes of the polyamines (PA) metabolism and two TF proteins (NF-kB p50 and c-myc) were searched for TFBS binding to NF-kB p50 and c-myc proteins. TFBS motifs were found in almost all structural genes been studied here, independently of presence or absence of corresponding TFBS in corresponding promoters. In total, number of both kinds of TFBS motifs in the structural genes is much more than in the promoters. In some cases, NF-KB-p50-binding DNA motifs are present only in the structural genes but not in the corresponding promoters, and the opposite cases are absent. Ratios between the same motifs numbers in the same pairs of genes were found to be quite different in human and mouse, showing that the patterns of the PA metabolism regulation network may be essentially different depending on the species and, probably, on the mice strain and human individual, i.e., on the genes allele. TFBS distribution between the human and mouse structural genes of the same name was similar, in contrast to the dramatic differences in their promoters. Based on these data and on the general regularities of evolution, the following hypothesis was proposed. Sequence of the gene regulatory structures creation is: structural gene — promoter — enhancers and silencers. TFBS in the structural genes are evolutionary old multifunctional instruments for the transcription control.

Keywords: transcription factor binding site, transcription control, metabolism control, evolution

Introduction

For today, there is extensive literature on the transcription factors (TF), their binding sites (TFBS) and evolution of both of these classes of the objects. However, all these publications deal with the special regulatory regions of a genome, especially gene promoters, or focus on evolution of TF themselves, or, at last, on global framework of transcription control [1 - 6]. And they all can't answer the following "childish" question: what are the TFBS located in the structural genes and how (besides location itself) they differ from ones located in the corresponding promoters?

At the same time, a few years ago [7] we have described the TFBS of NF-kB (especially, its p50 protein subunit) and c-myc TF in the introns of the structural genes encoding such proteins as elongation factors eEF1A1 and eEF1A2 and supposed these

TFBS may be involved in the splicing regulation.

Reasoning from the content of [7] (see its title in the "References") and contemporary situation in the TFBS investigations, it was of a special interest to search for NF-kB and c-myc TFBS in the promoters and structural genes encoding the main enzymes of the polyamines (PA) metabolism, as well as in the genes encoding the NF-kB and c-myc proteins themselves.

Materials and methods

Enzymes and their genes have been studied are listed in the Table 1. In each line of the table, under the gene's name, two numbers are given: the upper - number of nucleotides in a structural gene; the lower - the same in a corresponding promoter.

Table 1.

List of the genes being studied and their protein products

Number in order Gene Encoding protein and its function

Mouse Human

1 Odc1 6629 855 ODC1 8183 1328 Ornithine decarboxylase 1 (ODC), EC 4.1.1.17. Catalyzes the key step of the polyamines biosynthesis - conversion of L-ornithine to putrescine.

2 Oaz1 2634 983 OAZ1 4003 2250 The ODC antizyme. Inhibits ODC activity. Commonly, the antizyme protein expression increases under excess concentration of the polyamines in the cell.

3 Azin1 31857 1465 AZIN1 37898 1863 Anti-antizyme of ODC. Blocks the OAZ protein under deficient concentration of the polyamines in the cell.

4 Sat1 3323 348 SAT1 3066 670 Spermidine/spermine N1-acetyltransferase 1, diamine N-acetyltransferase, EC 2.3.1.57. Implements the first step of the polyamines catabolism - acetylation of the polyamines..

5 Smox 33401 897 SMOX 38968 931 Spermine oxidase, EC 1.5.3.16. (synonyms: PAOh1/SMO, AtPAO1, AtPAO4, SMO) is an enzyme with systematic name spermidine:oxygen oxidoreductase (spermidine-forming), which mainly catalyzes the following reaction: Spermine + O2 + H2O Spermidine + 3-aminopropanal + H2O2, thus being an agent of both catabolism and back-conversion of the polyamines.

6 Paox 8649 291 PAOX 12459 1714 Polyamine oxidase, EC 1.5.3.13. Mainly catalyzes the following reaction: N1-acetylspermine (or N1-acetylspermidine) + O2 + H2O Spermidine (or Putrescine) + 3-aminopropanal + H2O2 thus being an agent of both catabolism and back-conversion of the polyamines.

7 Nfkb1 106892 752 NFKB1 115973 1139 Protein p50 of NF-kB transcription factor. Function - binding to DNA NRE-sequences: GGGRNNYYCC, where R - pyrimidine (A, G); N — any nucleotide; Y- purine (C, T).

8 Myc 5020 3269 MYC 5365 3474+231=3705 Myc (c-Myc) gene codes for a transcription factor. The protein encoded by this gene is a multifunctional nuclear phosphoprotein involved in cell cycle progression, apoptosis and malignant transformation. This transcription factor binds to the E-box DNA sequence CACGTG. Some authors generalize this sequence up to CANNTG, where N — any nucleotide. C-myc protein expression is NF-KB-dependent.

Nucleotide sequences of the structural genes and their promoters were retrieved in the NCBI database (http://www. ncbi.nlm.nih.gov) and saved in the Microsoft Word format (.doc or .docx).

Search for TFBS was carried out using the "find in text" function of Microsoft Word in the following mode.

The GGGRNNYYCC decamer, where R - purine, Y -pyrimidine, N - any nucleotide, was accepted as a conventional NRE-sequence for p50 protein subunit included into the classic forms of the NF-kB TF (p50/p65 heterodimer and p50/p50 homodimer). 3'-GGG triplet and CC-5' dimer were accepted as the conservative structures. Only single variations (single deletion, single insertion, single exchange) in the RNNYY region (for example, RNYY, RRNNYY, YNNYY, RNNYR, etc) were taken into account. Complete list of such variations was arranged previously, and then each of them was searched for.

Similarly, the CACGTG hexamer was accepted as a conventional E-box sequence for c-myc TF. Since some authors generalize it to the CANNTG form, we have accepted the 3'-CA and TG-5' dimers as the conservative structures and took to account only single variations (deletion, insertion, exchange) in the CG dimer. At last, the CG^GC transformation was interpreted as "inner inversion". Complete list of such variations was arranged previously, and then each of them was searched for.

Note 1. A question about the conservative structures in the TFBS is of a special interest. Really, we can see now that some TFBS have conservative ends (our case) and some of them have conservative center (for example, 11-mer binding the ETS1 TF [4]). Lastly, conservatism of certain regions in TFBS sequence is a relative concept - at least in certain cases [1] - and in these cases it means only lower frequency of exchanges in these regions.

Note 2. We name the TFBS variations as "deletions", "insertions" or "exchanges", i.e., such as mutations are named commonly. But we can't know, are they real mutations or constitutional variations. Indeed, we can establish a real mutation only if we know that certain nucleotide sequence was previously without the variation we observe now and only later got it.

Results and discussion

At first, we must take into account that quantitative ratios seen in the Tables 2 and 3 may not be interpreted as general patterns for human and mice. Indeed, the nucleotide sequences we use characterize only one individual donor (in human) or only one inbred strain of mice, and, so, only one allele of each gene in each species. Moreover, we, for today, do not know how much these alleles differ from one another in their nucleotide sequence. Because of this, we present only summarized data in the main text. The detailed data (how many TFBS with deletions, insertions, etc. were found in each gene) one may obtain on request from the email address orlovaleks1955@ukr.net or

orlovaleks@rambler.ru .

What can we see in the tables?

Towards the TF motifs number itself. Thus, we can see the following (Table 2, 3).

TFBS motifs - both conventional and modified - for NF-kB p50 protein and for c-myc protein are present in almost all structural genes have been studied here, independently of presence or absence of corresponding TFBS in corresponding promoters. Only exclusions are human SAT1 gene and Oazl mouse (C57Bl/6) genes (none NF-kB p50 TFBS both in the structural gene and promoter).

Note 3. There are some reports [8, 9] showing presence of NF-kB p50 TFBS in human SAT1 promoter. But detailed analysis of the "Materials and methods" in these articles show the origin of the human DNA, been studied there, is quite different from the DNA described in NCBI database. So, this apparent collide with our data, indeed, confirms our hypothesis on different TFBS content in different alleles.

Quite different ratios between the same motifs numbers in the same pairs of genes in human and mouse show that the patterns of the PA metabolism regulation network may be essentially different depending on the species and, probably, on the mice strain and human individual, i.e., on the genes allele.

Table 2.

NF-KB-p50-binding DNA NRE motifs in the genes being studied

Gene Number of the motifs (in parentheses - "mutant")*, ** Density of the motifs location per 1 kb (1000 nucleotides)

Promoter Structural gene

Human

ODC1 0 (0) 0 3 (2) 0.37 (0.24)

OAZ1 6(5) 2.67 (2.22) 9(8) 2.25 (2.00)

AZIN1 0(0) 0 7(5) 0.18 (0.13)

SAT1 0(0) 0 0(0) 0

SMOX 0(0) 0 26(19) 0.67 (0.49)

PAOX 6(4) 3,50 (2.33) 6(6) 0.48 (0.48)

NFKB1 1(1) 0.88 (0.88) 19(13) 0.16 (0.11)

MYC 1(1) 0.27 (0.27) 4(4) 0.75 (0.75)

C57Bl/6 mice

Odc1 1(1) 1.17 (1.17) 3(3) 0.15 (0.15)

Oaz1 0(0) 0 0(0) 0

Azin1 0(0) 0 6(6) 0.19 (0.19)

Sat1 0(0) 0 1(1) 0.30 (0,30)

Smox 0(0) 0 8(6) 0.24 (0.18)

Paox 0(0) 0 6(5) 0.69 (0.58)

Nfkb1 1(1) 1.33 (1.33) 39(34) 0.36 (0.32)

Myc 1(1) 1.17 (1.17) 3(3) 0.15 (0.15)

Odc1 0(0) 0 0(0) 0

Notes. In this and previous table: * - the upper number - number of the motifs; the lower number - motifs density. ** - see Note 2 in Materials and methods.

Table 3.

C-myc-binding DNA E-box motifs in the genes being studied

Gene Number of the motifs (in parentheses - "mutant")*, ** Density of the motifs location per 1 kb (1000 nucleotides)

Promoter Structural gene

Human

ODC1 4(4) 3.01 (3.01) 42(39) 5.13 (4,77)

OAZ1 5(5) 2.22 (2.22) 11(11) 2.75 (2.75)

AZIN1 6(4) 3.22 (2.15) 143(142) 3.77 (3.75)

SAT1 2(2) 2.99 (2.99) 15(15) 4.89 (4.89)

SMOX 10(10) 10.74 (10.74) 211(209) 5.41 (5.36)

PAOX 8(8) 4.67 (4.67) 85(83) 6.82 (6.66)

NFKB1 2(2) 1.76 (1.76) 393(386) 3.39 (3.33)

MYC 8(8) 2.16 (2.16) 15(15) 2.80 (2.80)

C57Bl/6 mice

Odc1 6(6) 7.02 (7.02) 39(37) 5.88 (5.58)

Oaz1 2(2) 2.03 (2.03) 16(16) 6.08 (6.08)

Azin1 12(8) 8.19 (5.46) 110(109) 3.45 (3.42)

Sat1 2(2) 5.74 (5.74) 13(13) 3.91 (3.91)

Smox 1(1) 1.11 (1.11) 204(202) 6.11 (6.05)

Paox 1(1) 3.44 (3.44) 56(54) 6.47 (6.24)

Nfkb1 5(4) 6.65 (5.32) 535(523) 5.01 (4.89)

Myc 12(12) 3.06 (3.06) 18(18) 3.59 (3.59)

Odc1 6(6) 7.02 (7.02) 39(37) 5.88 (5.58)

Notes. In this and previous table: * - the upper number - number of the motifs; the lower number - motifs density. ** - see Note 2 in Materials and methods.

In total, number of NF-kB p50 TFBS motifs in the genes have been studied is much lower than number of c-myc TFBS motifs.

In total, number of both kinds of TFBS motifs in the structural genes is much more than in the promoters. In some cases, this number amounts to several tens (NF-kB p50 TFBS) or even several hundred (c-myc TFBS).

In total, number of the modified TFBS is much more than of the conventional ones.

Judging by number of the corresponding TFBS motifs, the human NFKB1 and MYC genes, as well as mouse Nfkb1 and Myc genes, have high level of both self- and cross-regulation.

It is notable that both human and mouse enzymes being responsible for both catabolism and back-conversion of the PA (SMOX and PAO) have, in total, comparatively very high number of both NF-kB p50 and c-myc TFBS motifs in their structural genes and promoters. This fact is in good agreement with a hypothesis that these metabolic pathway is comparatively evolutionary young shunt, realizing fine regulation of the intracellular PA content. Some less but also quite high number of these motifs is present in both human and mouse genes encoding the OAZ1 and AZIN1 proteins.

Towards density of the motifs location. If a certain TF molecule have got to a certain gene, we can evaluate the probability

measure (M) of the TF retaining in the gene's sphere of influence. This measure non-linearly depends on the corresponding TFBS number (N) in this gene and may be described with the following equation:

M=k1 Nk2 N/L k3 L (1),

in which k1 - constant of specific affinity of the TF to the TFBS; k2 - constant of influence of the TFBS density in the gene's region (this constant depends on the TF diffusion mobility); k3 - sum of the constants of hydrogen bond and three kinds of Van der Waals interactions between the TF and the nonspecific DNA regions; L - length of the gene (in bases, kilobases or any

other units).

Then, since the k123 constants must be determined experimentally for each concrete case, we may write, in the general case, the following:

M~N2 (2).

This measure may be interpreted as a control coefficient of this gene by this TF, in other words, as this-TF-dependent control factor of this gene. Distribution of the NF-kB p50-depended and c-myc-dependent control factors in the genes group have been studied in this work is present on the Fig. 1.

Fig. 1. Distribution of the NF-kB p50-depended and c-myc-dependent control coefficient in the group of the genes encoding the enzymes of the polyamines metabolism and p50 and c-myc proteins. A-D - in human donor's structural genes (B, D) and their promoters (A, C). E-H - in C57Bl/6 mouse structural genes (F, H) and their promotes (E, G). Each bar number marked under the X axis corresponds to the gene have been marked by this number in the Tables 1-3.

We shall not carry out detailed quantitative analysis of these distributions, especially because they present only single human donor and only single inbred line of mice. Let us view only some most interesting facts.

First of all, as we can see, the traditional (promoter-dependent) control pathways for the same metabolic and gene expression processes may be quite different in different mammal cells. Especially (Fig. 1 A, E), the classic form of the NF-kB TF controls the PA metabolism through OAZ and PAO in the human

donor's cells but through ODC - in C57Bl/6 mouse cells. In addition, NF-kB TF in the human cells controls p50 expression as well as the c-myc expression, but in the mouse cells - only p50 but not c-myc expression. C-myc TF (Fig. 1 C, G) controls the PA metabolism through all enzymes been studied here, but in essentially different quantitative relations. In the human cells, the main c-myc-controlled enzymes are ODC, SMOX and PAO, but in the mouse cells they are ODC and AZIN. As to the TF expression, c-myc in both human and mouse cells controls

preliminary self expression and some weaker - p50 expression.

In contrast to this, the distributions of both NF-kB p50-binding (Fig. 1 B, F) and c-myc-binding (Fig. 1 D, H) motifs between the structural genes of the human and mouse cells are much more similar one to another. These facts are of fundamental importance for the evolutionary interpretation of the present material.

What may mean this?

1. As it is generally known, one of the basic evolutionary patterns, both in organic and inorganic matter, is earlier creation of the substantial structures and their subsequent differentiation. Because of this, we suppose the regulatory regions are later evolutionary gains than a structural gene, and evolution has the following succession: structural gene — promoter — enhancers and silencers. Since, as it is also generally known, the evolutionary old adaptations are more stable than young ones, the similarity of the TFBS distribution between the human and mouse structural genes in contrast to the dramatic differences in their promoters may be an essential argument in favor of this hypothesis. In addition, we can see some cases when the NF-KB-p50-binding DNA NRE motifs are present only in the structural genes but not in the corresponding promoters (Table 1), and the opposite cases are absent. Then, several TFBS in the structural gene may be very old evolutionary adaptations to regulate transcription of the structural genes in absence of the promoters. Their existence itself indicates that, under contemporary conditions, they may function as a reserve mechanism of transcription control. It is logical to suppose this mechanism is more frequently realized in evolutionary old genes. Presence of these motifs in the introns constrains us to suppose some introns or their parts are evolutionary old prototypes of contemporary promoters. If a contemporary promoter is knocked down, these TFBS (if they are located lefter of the sequence encoding the enzyme's active center or antigenic determinant) may control transcription of evolutionary old enzyme's (antigen's) forms with some lower molecular mass. It is not improbable that expression of such old proteins is possible mainly in dis-differentiated, especially malignant cells.

2. On the other hand, it is known [10 - 12] that different parts of the same structural gene can be transcribed into mRNA for different proteins and peptides. This may be caused,

especially, by splicing, including splicing in the TF-encoding genes. It is most logical to suppose this phenomenon is provided by the TFBS being located too right to control the basic enzyme (antigen) transcription.

3. It also may be supposed that the structural gene's TFBS in any location permit TF to be not only initiator but also a blocker of transcription.

4. The modified TFBS may be the sites for DNA interaction with old, less stereospecific TF forms. Such TF, in contrast to their newest forms, must be less effective in attaining of the maximum reaction rate and specificity of its regulation, but more effective in the aspect of gradual transcription regulation by the simplest, exceptionally physical and chemical factors such as modulations of pH, ionic force, temperature, etc., not requiring any specific regulatory molecules (for example, PA with their specific binding site in the NF-kB p50 protein molecule).

5. At last, TFBS (especially their minor modes) located in the structural genes can play the same role in the wave genome control [13] as play the frets in the fingering on a stringed musical instrument. At that, TF play the same role as the musician's fingers.

6. As to the PA metabolism enzymes themselves, one can make the following conclusion. The well-known scheme of the PA metabolism regulation is only an integrative pattern, but concrete pathways in an individual organism strongly depend on an individual combination of the enzymes' genes alleles. We also suppose this situation is analogous in any multi-enzyme system.

What next?

Clearly, the ultimate aim of any TFBS investigations is to become familiar with transcription control mechanisms and use them in medicine and agriculture. To hasten this moment, the following top-priority steps must be done:

- to elaborate a special software for synchronous but differentiated search for all possible TFBS in the structural genes and their promoters, enhancers and silencers;

- to apply this software to extensive TFBS search in a whole genome of different inbred strains of mice and other eucaryotes, as possible;

- to perform intrastrain, interstrain, intraspecies and interspecies cluster analysis of the data obtained during the previous step.

References

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2. Berg G., Willmann S., Lässig M. Adaptive evolution of transcription factor binding sites // BMC Evolutionary Biology 2004, 4:42 doi:10.1186/1471-2148-4-42.

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4. Nguen T.T., Androulakis I.P. Recent Advances in the Computational Discovery of Transcription Factor Binding Sites // Algorithms 2009, 2, 582-605; doi:10.3390/a2010582

5. Nakagawa S., Gisselbrecht S. S., Rogers J. M., Hartl D. L., Bulyk M. L. DNA-Binding Specificity Changes in the Evolution of Forkhead Transcription Factors // Proceedings of the National Academy of Sciences 110, no. 30 (July 23, 2013): 12349-12354.

6. Cheatle Jarvela A.M., Hinman V.F. Evolution of transcription factor function as a mechanism for changing metazoan developmental gene regulatory networks // EvoDevo 2015, 6:3.

7. Orlovsky A.A., Zaletok S.P., Vislovukh A.A., Lukash T.A., Negrutskii B.S. Transcription factors NF-kB and c-myc and elongation factor eEF1A constitute a transparent cascade system being down-regulated by green tea polyphenols through inhibition of polyamines biosynthesis / In: Biologically active substances: fundamental and applied problems.- May 25-30, 2009.- Novy Svet, AR Crimea, Ukraine.- P. 366.

8. Babbar N., Hacker A., Huang Y., Casero R.A. Tumor necrosis factor alpha induces spermidine/spermine N1-acetyltransferase through nuclear factor kappaB in non-small cell lung cancer cells // J.Biol.Chem.- 2006.- 281(34).- P. 24182-24192.

9. Babbar N., Gerner E.W., Casero R.A. Induction of spermidine/spermine N1-acetyltransferase (SSAT) by aspirin in Caco-2 colon cancer cells // Biochem J. 2006 Feb 15; 394(Pt 1): 317-324. doi: 10.1042/BJ20051298

10. Talavera D., Orozco M., De la Cruz X. Alternative Splicing of Transcription Factors' Genes: Beyond the Increase of Proteome Diversity // Comparative and Functional Genomics.- Volume 2009, Article ID 905894, 6 pages.-doi:10.1155/2009/905894.

11. Faigenbloom L., Rubinstein N.D., Kloog Y., Mayrose I, Pupko T., Stein R. Regulation of alternative splicing at the singlecell level // Molecular Systems Biology 2015.- 11: 845. DOI 10.15252/msb.20156278. Published online: December 28, 2015.

12. Gawron D., Ndah E., Gevaert K, Van Damme P. Positional proteomics reveals differences in N-terminal proteoform stability // Molecular Systems Biology 2016.- 12: 858. DOI 10.15252/msb.20156662. Published online: February 18, 2016.

13. Гаряев П.П. Лингвистико-волновой геном. Теория и практика.- Киев: Институт квантовой генетики (Москва), 2009.- 217 с. (Garyaev P.P. Linguistic-and-wave genome. Theory and practice.- Kiev: Institute for quantum genetics (Moscow), 2009.- 217 p. (in Russian).

БОНИТИРОВКА ПОЧВИ ПО ЭКСПОЗИЦИИ И КУРТИЗНА СКЛОНОВ

Исматулло Умматович Урозбоев.

кандидат сельскохозяйственных наук, дотцент кафедры почвоведение, Гулистанский государственный университет

В статье излагается результаты опыта проведенных на староорошаемом типичном сероземе по выявлению крутизна и экспозиции склонов на плодородие почв. Доказано, пестроты мезо-, микрорельефа и микроклимата на различных экспозиций в хлопководстве приводит к потери урожая. По мере увеличения крутизны склона наблюдается повсеместное уменьшение урожайности хлопчатника и на основании этих данных составлены коэффициент корреляции.

Ключевые слова: бонитировка, рельеф, корреляция, агрорельеф, агроклимат, профиль, экспозиция, уклон, солнечных, теневых, микроклимат, морфология.

BONITATION SOIL ON AN EXPOSITION AND STEEPNESS OF SLOPES

Urazbaev I.U.

candidate of agricultural sciences, assistant Gulistan state university of Soil sience

In article is stated results of the experience called on on long irrigated typical siereozem on discovery steepness and exposures declivity on fertility of ground. It Is Proved, diversities of colors mezo-, microrelief and microclimate on different exposure in cotton growing brings about loss of the harvest. The ubiquitous reduction exists On measure of the increase the of the declivity to productivities of the cotton plant and on the grounds of these given is formed factor to correlations.

Key words: bonitation, relief, correlation, agrorelief, agroclimate, structure, exposition, gradient, solar, shadow, microclimate, morphology.

Введение: Почва как самая верхняя оболочка земной поверхности находится в тесной взаимосвязи с рельефом местности. Роль рельефа как фактора почвообразования и агроэкологии состоит главным образом в том, что он перераспределяет по поверхности земли солнечную энергию (тепло и свет) и атмосферную влагу. В условиях расчлененного рельефа участки земной поверхности различно ориентированные к странам света, получают различное количество энергии солнца. Температура приземного слоя атмосферы значительно колеблется на различных склонах. Солнечные лучи более вертикально падают на поверхность южного и восточного склонов что приводит к лучшему их обогреванию. Даже в условиях слабовыраженных волнистых предгорных равнин, где протяженность склонов небольшая и поверхность относительно пологая, на «солнечных» склонах травы появляются на 5-7 дней раньше, чем на «теневых». Почвы на «солнечных» склонах поспевают для вспашки на 7-10 дней раньше, чем на «теневых».

По мнению В.Н.Ли и С.М.Елюбаева [2, 57-59] на различных элементах рельефа образуются почвы с различными свойствами, что определяет пестроту почвенного покрова в условиях расчлененного рельефа и урожая даже в пределах одного поливного участка.

И.И. Карманов и Т.А.Фриев [1, 3-6] предлагают учитывать влияние рельефа на плодородие почвы через показа-

тели тепло и влагообеспеченности и континентальности климата, слагающихся на склонах различной крутизны и экспозиции.

Объект и методика исследований: Объектами исследований в данной работе послужила орошаемый типичный серозём на лессовидных покровных суглинках и закономерно образуемые ими элементарные почвенные структуры [ЭПС] Ташкентского оазиса.

В качестве основных в работе были использованы следующие методы: сравнительно-географический, вложенных ключей, статистико-картографический, лабораторный, полевые опыты. Для математической обработки полученных результатов был использован информационно-статистический анализ. Сущность использования нами в работе сравнительно-географического метода заключалась в параллельном, сравнительном изучении в разных пунктах почв и рельефа и в анализе их соотношений. Это определяется представлением о том, что все природное компоненты в пределах генетически однородной части земной поверхности находятся в тесной взаимосвязи, образуя единое природное целое-ландшафт.

К числу определяющих принципов организации поч-венно-геоморфологических профилей нами были отнесены следующие: 1) профиль должен проходить от самого высокого места территорий к самому низкому; 2) масштаб