Induction of a bZIP Type Transcription Factor and Amino Acid Catabolism-Related Genes in Soybean Seedling in Response to Starvation Stress

To address roles of bZIP transcription factors on regulation of amino acid catabolism under autophagy-induced plant cells, we examined the effect of nutrient starvation on the expression of low energy stress-related transcription factor homologs, GmbZIP53A and GmbZIP53B, and amino acid catabolism-related genes in soybean (Glycine max (L.) Merr.). Sucrose starvation treatment significantly enhanced the expressions of GmbZIP53A, but not GmbZIP53B asparagine synthase (GmASN1), proline dehydrogenase1 (GmProDH), and branched chain amino acid transaminase 3 (GmBCAT3). GmbZIP53-related immunoreactive signals were upregulated under severe starvation with sucrose starvation and protease inhibitors, while 3% sucrose and sucrose starvation had no or marginal effects on the signal. Profiles of induction of GmASN1, GmProDH and GmBCAT3 under various nutrient conditions were consistent with the profiles of GmbZIP53 protein levels but not with those of GmbZIP mRNA levels. These results indicate that GmbZIP53 proteins levels are regulated by posttranslational mechanism in response to severe starvation stress and that the increased protein of GmbZIP53 under severe starvation accelerates transcriptional induction of GmASN1, GmProDH, and GmBCAT3. Furthermore, it is conceivable that decrease of branched chain amino acid level by the BCAT-mediated degradation eventually enhances autophagy under severe starvation.

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Mechanisms contributing to muscle-wasting in acute uremia: activation of amino acid catabolism.

Journal of the American Society of Nephrology ◽

10.1681/asn.v93439 ◽

1998 ◽

Vol 9 (3) ◽

pp. 439-443

Author(s):

S R Price ◽

D Reaich ◽

A C Marinovic ◽

B K England ◽

J L Bailey ◽

...

Keyword(s):

Amino Acid ◽

Muscle Wasting ◽

Essential Amino Acids ◽

Mrna Levels ◽

Amino Acid Catabolism ◽

Metabolic Defects ◽

Branched Chain Amino Acid ◽

Branched Chain ◽

Ketoacid Dehydrogenase ◽

And Control

Acute uremia (ARF) causes metabolic defects in glucose and protein metabolism that contribute to muscle wasting. To examine whether there are also defects in the metabolism of essential amino acids in ARF, we measured the activity of the rate-limiting enzyme for branched-chain amino acid catabolism, branched-chain ketoacid dehydrogenase (BCKAD), in rat muscles. Because chronic acidosis activates muscle BCKAD, we also evaluated the influence of acidosis by studying ARF rats given either NaCl (ARF-NaCl) or NaHCO3 (ARF-HCO3) to prevent acidosis, and sham-operated, control rats given NaHCO3. ARF-NaCl rats became progressively acidemic (serum [HCO3] = 21.3 +/- 0.7 mM within 18 h and 14.7 +/- 0.8 mM after 44 h; mean +/- SEM), but this was corrected with NaHCO3. Plasma valine was low in ARF-NaCl and ARF-HCO3 rats. Plasma isoleucine, but not leucine, was low in ARF-NaCl rats, and isoleucine tended to be lower in ARF-HCO3 rats. Basal BCKAD activity (a measure of active BCKAD in muscle) was increased more than 17-fold (P < 0.01) in ARF-NaCl rat muscles, and this response was partially suppressed by NaHCO3. Maximal BCKAD activity (an estimate of BCKAD content), subunit mRNA levels, and BCKAD protein content were not different in ARF and control rat muscles. Thus, ARF increases branched-chain amino acid catabolism by activating BCKAD by a mechanism that includes acidosis. Moreover, in a muscle-wasting condition such as ARF, there is a coordinated increase in protein and essential amino acid catabolism.

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