Ribosomal proteins of mouse kidney: Normal status and during compensatory renal hypertrophy

1977 ◽  
Vol 17 (1) ◽  
pp. 25-30
Author(s):  
Thomas E. Northrup ◽  
D. Irwin ◽  
Ronald A. Malt
1980 ◽  
Vol 188 (1) ◽  
pp. 229-235 ◽  
Author(s):  
W T Melvin ◽  
A Kumar ◽  
R A Malt

The rate of synthesis of ribosomal proteins was investigated as an index of the rate of production of ribosomes in mouse kidney during the first few days after contralateral nephrectomy. Compensatory renal hypertrophy was not associated with a major increase in the synthetic rate of ribosomal proteins and rRNA. Instead, the ratio of the rate of ribosomal-protein synthesis to that of total protein synthesis remained nearly constant. The conformation of glutaraldehyde-fixed ribosomes and ribosomal subunits was unchanged. During the early stages of compensatory renal hypertrophy the accretion of rRNA is due largely to conservation of ribosomes that would otherwise have been degraded.


1976 ◽  
Vol 69 (3) ◽  
pp. 548-556 ◽  
Author(s):  
W T Melvin ◽  
A Kumar ◽  
R A Malt

After removal of one mouse kidney, compensatory hypertrophy in the remaining kidney is marked in 2 days by a 20% average increase in ribosomal RNA (rRNA) per cell. Both 28S and 18S RNA are conserved during the initial stages of compensatory renal hypertrophy to an extent sufficient to account for the rest of the observed accumulation of rRNA. Like some cultured cells, the kidney conserves rRNA during physiological growth.


1979 ◽  
Vol 237 (5) ◽  
pp. R360-R365
Author(s):  
A. J. Ouellette ◽  
R. A. Malt

To examine the regulatory role of mRNA in compensatory renal hypertrophy, the accumulation and decay of [3H]orotic acid in poly(A)-containing mRNA in mouse kidney was analyzed after unilateral nephrectomy during the period of maximal rRNA accretion. The distribution of radioactivity between newly synthesized poly(A)-containing and poly(A)-lacing polysomal RNA was altered, but no differences in mRNA half-life were observed in growth compared with effects of sham nephrectomy. Radioactivity in polysomal polyadenylated RNA was diminished by approximately 25% during growth where mice were labeled after nephrectomy, but if mice were labeled 18 h before operation, no difference was noted. Thus, accumulation of newly synthesized poly(A)-containing mRNA relative to RNAs that lack poly(A) is changed early in the course of renal hypertrophy. This noncoordinate regulation may represent a control mechanism effective early in induced cell growth involving mRNAs that lack poly(A).


1987 ◽  
Vol 253 (4) ◽  
pp. C506-C513 ◽  
Author(s):  
A. J. Ouellette ◽  
R. Moonka ◽  
A. D. Zelenetz ◽  
R. A. Malt

Ribosomal synthesis was studied at the transcriptional and translational levels to investigate the mechanisms of ribosome accretion during compensatory renal hypertrophy. As measured by in vitro transcriptional runoff comparisons 6-48 h after surgery, nuclei from the kidney remaining after contralateral nephrectomy show an increase of up to 150% in the rate of synthesis of ribosomal precursor RNA. The rate of rDNA transcription is 40-50% greater than control values as early as 6 h after nephrectomy; by 48 h, the rate returns to normal. In contrast to the stimulated transcription of rDNA and accretion of rRNA, the steady-state levels and the cytoplasmic distribution of ribosomal protein mRNAs S16 and L10 remain unchanged during induced renal growth. Thus coordinate production of adequate protein for increased assembly of ribosomes during induced renal growth appears to be accomplished by increasingly efficient translation of existing ribosomal protein mRNAs or by post-translational stabilization of ribosomal proteins. The rate of rDNA transcription may be regulated by accelerating the transcription of already functioning genes or, more likely, by recruiting transcription units that are transcriptionally inactive in the normal kidney.


1977 ◽  
Vol 68 (7) ◽  
pp. 644-651 ◽  
Author(s):  
Takashi Umeda ◽  
Kenkichi Koiso ◽  
Hisao Takayasu

1967 ◽  
Vol 98 (5) ◽  
pp. 548-551 ◽  
Author(s):  
James W. Thompson ◽  
Bernard Lytton

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