The Physiology and Mechanism of Growth

Author(s):  
Adda Grimberg ◽  
Moshe Phillip ◽  
Jarod Wong ◽  
S. Faisal Ahmed
Keyword(s):  
2007 ◽  
Vol 178 (15-18) ◽  
pp. 1039-1047 ◽  
Author(s):  
H GALAI ◽  
M PIJOLAT ◽  
K NAHDI ◽  
M TRABELSIAYADI

1970 ◽  
Vol 131 (2) ◽  
pp. 367-375 ◽  
Author(s):  
Arthur I. Grayzel ◽  
Carolyn Beck

The mechanism of growth stimulation in allogeneic lymphocytes mixed in vitro was studied at the cell level by means of cytophotometric techniques. A pronounced increase in fluorescence intensity of fixed and acridine orange (AO) stained lymphocytes was observed as soon as after 1–3 hr in mixed culture. No increase in the amount of DNA took place during this time. The higher fluorescence intensity was due to an increased accessibility of AO binding sites in the deoxyribonucleoprotein (DNP) complex, most probably as a result of weakened bonds between the DNA and the protein moiety in the DNP complex. Similar DNP changes have been found in other systems of growth stimulation and may be one prerequisite for later induction of cellular synthetic processes. Increased AO binding only occurred when the lymphocyte donors were incompatible at the major histocompatibility locus (HL-A); there was no change in AO binding in cases of HL-A identity. The AO binding reaction probably reflects a specific recognition of HL-A antigens, whereas other antigenic discrepancies between the individuals do not seem to cause an analogous response.


2021 ◽  
Author(s):  
Lisa P Deliu ◽  
Deeshpaul Jadir ◽  
Abhishek Ghosh ◽  
Savraj S Grewal

The regulation of ribosome function is a conserved mechanism of growth control. While studies in single cell systems have defined how ribosomes contribute to cell growth, the mechanisms that link ribosome function to organismal growth are less clear. Here we explore this issue using Drosophila Minutes, a class of heterozygous mutants for ribosomal proteins (Rps). These animals exhibit a delay in larval development caused by decreased production of the steroid hormone ecdysone, the main regulator of larval maturation. We found that this developmental delay is not caused by decreases in either global ribosome numbers or translation rates. Instead, we show that they are due in part to loss of Rp function specifically in a subset of serotonin (5-HT) neurons that innervate the prothoracic gland to control ecdysone production. We found that these 5-HT neurons have defective secretion in Minute animals, and that overexpression of synaptic vesicle proteins in 5-HTergic cells can partially reverse the Minute developmental delay. These results identify a cell-specific role for ribosomal function in the neuroendocrine control of animal growth and development.


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