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Transcription factor LbUBC positively regulates salt gland development and salt tolerance by directly binding to the LbTTG1 promoter and repressing its transcription.

KEY MESSAGE:: LbUBC enhances salt tolerance by promoting salt gland development via repressing LbTTG1, revealing a synergisticregulatory mechanism in Limonium bicolor. In the context of increasingly severe soil salinization, salt-tolerant genetic resources from halophytes show great application potential. In particular, the recretohalophyte Limonium bicolor, which possesses specialized salt gland structures, has become a key model for deciphering the molecular mechanisms underlying salt tolerance and salt gland development. In this study, using LbTTG1-overexpressing and -silenced lines, we demonstrate that LbTTG1 negatively regulates salt-gland development and salt tolerance. Through yeast one-hybrid, EMSA, and dual-luciferase assays, Lb7G33228 (LbUBC) was screened and verified as an upstream transcriptional regulator of LbTTG1. LbUBC enhances salt tolerance in L. bicolor by positively regulating salt-gland development, verified using LbUBC silence and overexpression strains. Interestingly, LbUBC represses the expression of its downstream target LbTTG1, thereby releasing the inhibitory effect of LbTTG1 on salt-gland development. In this manner, LbUBC positively regulates salt-gland development, achieving a dynamic balance in the regulation of salt-gland development and salt tolerance in L. bicolor. This study reveals a synergistic regulatory mechanism involving multiple genes, offering new insights for comprehensively dissecting the molecular regulatory network of salt-gland development.

Salt Tolerance

Identification and analysis of HD-ZIP transcription factors that regulate salt gland development and salt tolerance in Limonium bicolor.

Soil salinity severely constrains agricultural production. Elucidating the salt-tolerance mechanisms of halophytes can provide innovative approaches for improving the salt tolerance of crop plants. In this study, we performed genome-wide identification and analysis of 36 LbHDZ genes encoding homeodomain-leucine zipper (HD-ZIP) transcription factors in Limonium bicolor, a typical recretohalophyte that excretes excess salt ions through specialized salt glands. Expression profiling across different stages of salt gland development, as well as in various tissues under salt stress, indicated that multiple LbHDZ genes are involved in regulating salt gland development and salt tolerance. Among these genes, LbHDZ14 (a member of the HD-ZIP II subfamily) exhibited sustained high expression during the critical period of salt gland formation, while its transcript levels were significantly downregulated in leaves and roots under salt stress. Subsequent experiments demonstrated that LbHDZ14 is localized in the nucleus and negatively regulates salt gland density and salt tolerance by directly binding to the promoter of LbGDSL, a positive regulator of salt gland development. In conclusion, this study reveals the expression patterns of LbHDZ genes in L. bicolor, characterizes the functional mechanism of LbHDZ14, further elucidates the regulatory network underlying salt gland development, and provides candidate genes for enhancing crop salt tolerance.

Plumbaginaceae

[Certain changes in the water-electrolyte metabolism in desoxycorticosterone acetate salt hypertension in rats adapted to high altitude hypoxia].

In the course of the development of desoxycorticosterone-acetate-salt hypertension the animals were noted to display high appetite of sodium chloride, a considerable increase of the weight of the heart, kidneys and adrenal glands, of the diameter of the glomeruli and the surface of the cortical and medullar zones of the kidneys, a decrease of the sodium and potassium gradient in the renal tissue. Adaptation to hypoxy is noted so cause a decrease in the interventricular factor, in the width of the glomerular zone of the adrenal glands, in the sodium concentration in the erythrocytes, an increase in the mass of the medullar layer of the kidneys, and an increase in the sodium and potassium gradients. When adaptation to hypoxy is combined with the effect of desoxycorticosterone-acetate-salt, hypertension develops to a lower degree than in non-adapted animals.

Adaptation, Physiological

Effect of cadmium on salt hypertension in rats.

The suggestion that cadmium-induced hypertension in rats might be due to renal sodium retention, known to result from Cd treatment, was examined. Young female rats were given a regimen of intraperitoneal cadmium treatments reported to cause hypertension reliably within a month. They were sensitized to the development of salt hypertension by removal of one kidney and then given 1 percent saline solution to drink. Over a five-week period, experimental animals consistently drank more saline than controls, despite which fewer of them became hypertensive, with the result that the average systolic pressure of controls finally reached the hypertensive range, whereas the experimental group remained normotensive. Cadmium treatment had no detectable effect on growth, the hemogram, serum Na and K, or the weight of liver, kidney, heart, spleen, thymus, or adrenal glands. There was thus no evidence that cadmium caused any adverse constitutional or hemodynamic effects, but it appeared to retard the development of salt hypertension. The results do not support the suggestion that the hypertensive effects of cadmium are modulated by sodium-retaining influences on the kidney.

Animals

Peripheral and central catecholaminergic neurons in genetic and experimental hypertension in rats.

1. Activity of peripheral and central catecholaminergic neurons was studied in spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)-salt hypertensive rats. 2. In young SHR (4 weeks) the plasma values of bpth noradrenaline and dopamine-beta-hydroxylase activity were increased compared with those of normotensive rats of the Wistar/Kyoto strain. Total catecholamines (mostly adrenaline) were not significantly different. 3. In the adrenal glands of 2-weeks-old and 4-weeks-old SHR activities of tyrosine hydroxylase, dopamine-beta-hydroxylase, phenylethanolamine-N-methyl transferase were decreased, compared to Wistar/Kyoto rats. 4. The adrenaline-forming enzyme was elevated in the A1 and A2 regions of the brain stem of 4-weeks-old SHR and in the A1 region of adult DOCA-salt hypertensive rats. 5. In the adrenal glands of adult DOCA-salt hypertensive rats tyrosine hydroxylase activity was increased. 6. These results implicate peripheral noradrenaline-containing neurons and central adrenaline-containing neurons in the development of genetic and experimental hypertension in rats.

Adrenal Glands

Effects of ethacrynic acid on ion transport and energy metabolism in slices of avian salt gland and of mammalian liver and kidney cortex.

Ethacrynic acid greatly inhibited net transport of ions and aerobic, energy-conserving metabolism in slices of avian salt gland, rat liver, and rat and guinea-pig kidney cortex. The effects of increasing concentrations of ethacrynic acid on the transport of Na+, K+ and Cl- ran closely parallel to its effects on tissue ATP levels and respiration. The concentration needed for maximal inhibition of transport reduced ATP levels by 80--90%. Respiration was reduced by 80--90% in salt gland and kidney cortex, and by a maximum of 30% in liver slices. The effects of low concentrations of ethacrynic acid required time to become fully manifest in some tissues, and the development of transport inhibition followed a similar course to decline of respiration and ATP levels. Ca2+ extrusion by liver cells was inhibited by ethacrynic acid. The concentration dependence of the inhibition was similar to that shown by the other transport systems inhibited. There was no distinction evident between the sensitivity of Na+ extrusion and of K+ accumulation to the diuretic. Lactate production increased as respiration decreased in the presence of increasing concentrations of ethacrynic acid. We conclude that ethacrynic acid acted primarily as an inhibitor of mitochondrial respiration and ATP synthesis in the tissue slices, and that inhibition of ion transport was a nonspecific consequence of the failure of the energy supply.

Adenine Nucleotides

The metabolic effects of sodium depletion in calves on salt appetite assessed by operant methods.

1. Sodium deficiency was induced in calves by unilateral exteriorization of the parotid duct, the continual loss of alkaline saliva from the body to the environment causing negative sodium balance. 2. The metabolic effect of negative sodium balance was seen in statistically significant reduction in plasma sodium and blood bicarbonate, together with marked acidosis and reduced plasma osmolality. 3. The homoeostatic response to sodium depletion was associated with a reversal of sodium/potassium ratio in parotid saliva and a reduction of the rate of secretion. Appetite diminished. The extracellular fluid was halved as marked diuresis developed with considerable weight loss. Urinary and faecal sodium was reduced to zero. 4. On restoration of sodium balance by allowing the calves to drink sodium bicarbonate solutions the metabolic deviations were eliminated. 5. During sodium depletion the parotid gland was able to respond to transient reflex stimulation by increasing flow rate and the sodium concentration of the saliva. 6. When sodium depleted, the calves became restless and agitated and would run from the home pen to the operant procedure stand. The sodium depleted animals readily pressed a panel for sodium bicarbonate rewards in direct proportion to the degree of sodium imbalance. When the balance was restored the motivation to work for sodium bicarbonate disappeared. 7. The motivation which developed during sodium depletion was directed specifically towards the sodium ion. Lithium was an exception to this rule and sodium carbonate was aversive. 8. It is possible that in sodium depletion the glottal sodium taste receptors develop an enhanced threshold for sodium ions because of the reduced sodium content of the saliva. This effect would be abolished when the content of sodium was restored in saliva. 9. The correlation of operant reactions and sodium depletion suggests that the consequential metabolic effects activate changes in the central nervous system. 10. The metabolic changes which develop in parallel with the severity of the sodium deficit appear to be able to evoke behavioural changes with increase in salt appetite directed towards restoration of sodium balance.

Animals

Selective reduction of adrenal medulla response to angiotensin induced by suppression of renin-angiotensin.

Angiotensin II (AII) induced an increase of adrenaline (A) release from rat adrenal glands in vitro. The response of the adrenal glands was completely abolished 22--24 h after bilateral nephrectomy. Adrenal glands from DOCA-salt-treated rats did not respond to AII as well, whereas adrenal glands from rats treated with furosemide and a low salt diet retained this response. High potassium in the medium increased significantly the release of A from in vitro incubated adrenal glands of nephrectomized rats from 0.43 +/- 0.04 to 0.63 +/- 0.06 microgram/gland and salbutamol (in calcium-free medium) increased the release from 0.34 +/- 0.03 to 0.43 +/- 0.03 microgram/gland. These results indicate that the adrenal medulla develops subsensitivity to AII in vitro, following a reduction in levels of this agonist in vivo.

Adrenal Medulla

[Mineral saturation, ossification and synostosis of the hand bones in adolescents and youth].

The results on X-ray densitometric studies of the hand bones in adolescent and young people at the age of 10--17 years (369 persons in all) are presented in the work. Processes of mineralization, ossification and synostosis, as the investigation has demonstrated, are closely connected with each other. From the beginning of ossification in the pisiform and sesamoid bones of the first metacarpophalageal joint (11--12 years of age) up to the completion of synostosis in short tubular bones of the hand (15--16 years of age), a decrease of mineral salts is noted in osseous tissue. Hence, accumulation of mineral salts in skeleton of children and adolescent persons does not occur smoothly, but rather distinctly reflects those functional changes which take place in the adolescent organism when the genital glands begin their increased activity.

Absorptiometry, Photon

[Chronobiologic aspect of the mechanism of action of lithium salts in experimental alcoholism].

Ethanol, used for 2 months in a 5% solution, disorganized the circadian cycle of the hystophysiologic activity of the rat epiphysis. During prolonged (course) administration in the doses close to those used at the clinic lithium chloride normalized the mentioned changes and also prevented their development in case of joint two-months use of ethanol and lithium salt. This effect of the drug correlates with the inhibition or prevention of the ethanol preference development observed under these perimental conditions. A possible interrelationship between the discovered capacity of lithium salt to normalize the chronobiological derangements of the epiphysis and clinical efficacy of these salts in alcoholism and other affective periodical disorders is discussed.

Alcoholism

[Ultrastructure of the secretory parenchyma of the postanal gland of the coelacanth, Latimeria chalumnae Smith].

Latimeria chalumnae Smith, the only surviving crossopterygian, possesses a well-developed, unpaired, postanal gland whose function is as yet undocumented. The availability of tissues suitable for ultrastructural and histochemical studies from the recent International Comores Expedition has permitted a reappraisal of the comparative morphology and functional hypotheses relating to the postanal gland. The richly vascularized tubuloacinar postanal gland is composed of cells which show the characteristic specializations of active ion transport. These include complex and extensive development of basal and lateral cell membrane infolding (cisternae) which are closely associated with numerous large, dense mitochondria. Histochemical studies have shown a high level of ATPase activity within the gland cells. These features of the postanal gland correlate well with those of the rectal glands of elasmobranchs and suggest a similar role in ion excretion and osmoregulation.

Animals

Development pharmacokinetics of the posterior pituitary hormones.

Arginine vasotocin, arginine vasopressin, and oxytocin play a critical role in the stimulation of labor and delivery and in salt and water homeostasis in the newborn infant. The authors present information on their chemistry, secretion, and metabolism, and discuss the clinical effects upon target organs of their presence or absence.

Animals

[Argyriasis. Report of a case (author's transl)].

A case of argyriasis in a 45-year-old woman is reported. When the patient was 34 she took for a period of 25 months a silver-containing pharmacological product (colloidal silicon with 0.5 percent of silver) in order to treat an intestinal dyspepsia with diarrheic episodes. A few months after discontinuing the treatment a cutaneous pigmentation of a greyish-blue color extending over the whole body, developed. There was also discoloration of the nails, hair, and of the oral and gingival mucosae. The differential diagnosis with other conditions that also develop anomalies of cutaneous pigmentation was established. It is thought that the appearance of the silver poisoning is due to different factors such as the quantity of silver intake, the individual sensitivity to the metal, and the greater or lesser period of exposure to sunlight. The importance of the skin biopsy in order to confirm the diagnosis is commented on. Typical pathologic findings include the presence of silver granules in the basal membrane of sudoriparous glands, around the pilosebaceous follicles, and in the connective tissue. Lastly, the authors insist on the necessity to avoid the prescription of silver-salt containing drugs as far as possible, since the cutaneous pigmentation is irreversible.

Argyria

Ultrastructure and ATPase activity of the rectal gland of the chondrichthyean fish Hydrolagus colliei (Holocephali).

The anatomy, histology, ultrastructure and ATPase activity of the intramural rectal gland of the chondrichthyean Hydrolagus colliei, are described. The cells of the rectal gland of Hydrolagus demonstrate the same well developed lateral and basal cisternae, elongate mitochondria and luminal border as those of their elasmobranch counterparts. ATPase activity within the rectal gland of Hydrolagus is as intense as that in a number of elasmobranchs examined in the course of the study. Despite its primitive intramural location the rectal gland of Hydrolagus represents a homolog of the more specialized and better known elasmobranch gland and appears as well suited for cation excretion.

Adenosine Triphosphatases

[Familial glucocorticoid insufficiency (author's transl)].

Familial glucocortivoid insufficiency--also called hereditary lack of response of the adrenals to ACTH-has not yet been described in Europe. Isolated glucocorticoid insufficiency combined with intact secretion of aldosterone and high plasma level of ACTH are characteristic. The diagnostic difficulties are demonstrated by the deaths before diagnosis of 13 siblings of 21 patients from 9 families. One such family is described. The first of 3 children died at the age of 3-1/2 years after a two day illness interpreted as encephalitis. Another boy, aged 4-1/2 years, had a hypoglycemic attack. 3 months later he died in status epilepticus after a short feverish illness. At autopsy the adrenals were very small. Histologically only the glomerulous zone was developed. An the hypophysis there was hyperplasia of the R cells producing ACTH. The 6 year old sister had been pronouncedly pigmented from the age of a few months onwards. Age in terms of height and bone development corresponded to 8-1/2 and 7-1/2 years. After intravenous insulin and synacthen plasmacorticoids could not be found. With normal and low supply of salt, the following data were found: Renin-activity 2.9 and 5.6 ng/ml p.h. respectively; rate of aldosterone secretion 62.6 and 151.5 mug/24 hrs.; average aldosterone plasma concentration 9.39 and 27.7 ng/100 ml respectively; MCR 666 and 5471 p/24 hrs. Plasma ACTH in this patient (5086--7200 pg/ml) and, post mortem, in her brother (8100 pg/ml), were extremely reaised.

Adrenal Glands

Dissociation between cortisol-induced pycnosis and inhibition of [3H]uridine incorporation in rat thymocytes.

Treatment of rat thymocytes with cortisol induced an inhibition of [3H]uridine incorporation after 30-90 min, an accumulation of pycnotic cells after 90 min, and a decrease in cell viability after several hours. No cortisol-resistant cells could be distinguished, and dose-response curves for a number of glucocorticoids showed a correlation to the saturation of the glucocorticoid receptors. The pycnotic effect of cortisol increased between pH 5.2--7.0 in parallel with a stimulation of the spontaneous development of pycnotic cells. The cortisol-induced accumulation of pycnotic cells and inhibition of [3H]uridine incorporation varied independently as a function of the cell density, and in a glucose-salt medium only the pycnotic effect of cortisol became inhibited. The inhibition of [3H] uridine incorporation is therefore not an integral part of the pycnotic change of the cells. The glucocorticoid sensitivity was found to increase with the age of the animals, before the onset of thymus involution.

Animals

Characteristics of the dephosphorylated form of phosphorylase purified from rat liver and measurement of its activity in crude liver preparations.

The phosphorylated form of liver glycogen phosphorylase (alpha-1,4-glucan : orthophosphate alpha-glucosyl-transferase, EC 2.4.1.1) (phosphorylase a) is active and easily measured while the dephosphorylated form (phosphorylase b), in contrast to the muscle enzyme, has been reported to be essentially inactive even in the presence of AMP. We have purified both forms of phosphorylase from rat liver and studied the characteristics of each. Phosphorylase b activity can be measured with our assay conditions. The phosphorylase b we obtained was stimulated by high concentrations of sulfate, and was a substrate for muscle phosphorylase kinase whereas phosphorylase a was inhibited by sulfate, and was a substrate for liver phosphorylase phosphatase. Substrate binding to phosphorylase b was poor (KM glycogen = 2.5 mM, glucose-1-P = 250 mM) compared to phosphorylase a (KM glycogen = 1.8 mM, KM glucose-1-P = 0.7 mM). Liver phosphorylase b was active in the absence of AMP. However, AMP lowered the KM for glucose-1-P to 80 mM for purified phosphorylase b and to 60 mM for the enzyme in crude extract (Ka = 0.5 mM). Using appropriate substrate, buffer and AMP concentrations, assay conditions have been developed which allow determination of phosphorylase a and 90% of the phosphorylase b activity in liver extracts. Interconversion of the two forms can be demonstrated in vivo (under acute stimulation) and in vitro with little change in total activity. A decrease in total phosphorylase activity has been observed after prolonged starvation and in diabetes.

Adenosine Monophosphate