Ferritin gene expression is developmentally regulated and induced by heat shock in sea urchin embryos

1993 ◽  
Vol 14 (1) ◽  
pp. 58-68 ◽  
Author(s):  
A. A. Infante ◽  
D. Infante ◽  
J. Rimland
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Sea Urchin ◽  
Developmentally Regulated ◽  
Sea Urchin Embryos ◽  
Ferritin Gene

Synthesis of ?heat shock? proteins in sea urchin embryos

1980 ◽  
Vol 4 (1) ◽  
pp. 69-74 ◽  
Author(s):  
G GIUDICE ◽  
M ROCCHERI ◽  
M DIBERNARDO
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Sea Urchin ◽  
Sea Urchin Embryos ◽  
Shock Proteins

Acquisition of thermotolerance in sea urchin embryos correlates with the synthesis and age of the heat shock proteins

1986 ◽  
Vol 19 (3) ◽  
pp. 173-177 ◽  
Author(s):  
G. Sconzo ◽  
M.C. Roccheri ◽  
M. La Rosa ◽  
D. Oliva ◽  
A. Abrignani ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Sea Urchin ◽  
Sea Urchin Embryos ◽  
Shock Proteins

Expression and structural analysis of heat-shock genes in sea urchin embryos P. lividus

1989 ◽  
Vol 27 ◽  
pp. 19
Author(s):  
G. Sconzo ◽  
M. LaRosa ◽  
M.C. Roccheri ◽  
M.G. Ferraro ◽  
D. Buccheri ◽  
...  
Keyword(s):  
Structural Analysis ◽  
Heat Shock ◽  
Sea Urchin ◽  
Heat Shock Genes ◽  
Sea Urchin Embryos

scholarly journals Inducible expression of a cloned heat shock fusion gene in sea urchin embryos.

1984 ◽  
Vol 81 (23) ◽  
pp. 7490-7494 ◽  
Author(s):  
A. P. McMahon ◽  
T. J. Novak ◽  
R. J. Britten ◽  
E. H. Davidson
Keyword(s):  
Heat Shock ◽  
Sea Urchin ◽  
Fusion Gene ◽  
Inducible Expression ◽  
Sea Urchin Embryos

scholarly journals Proteolysis of the major yolk glycoproteins is regulated by acidification of the yolk platelets in sea urchin embryos

1992 ◽  
Vol 117 (6) ◽  
pp. 1211-1221 ◽  
Author(s):  
SK Mallya ◽  
JS Partin ◽  
MC Valdizan ◽  
WJ Lennarz
Keyword(s):  
Early Development ◽  
Sea Urchin ◽  
Ph Value ◽  
Total Protein Content ◽  
Developmentally Regulated ◽  
Cell Stage ◽  
Ph Optimum ◽  
Sea Urchin Embryos

The precise function of the yolk platelets of sea urchin embryos during early development is unknown. We have shown previously that the chemical composition of the yolk platelets remains unchanged in terms of phospholipid, triglyceride, hexose, sialic acid, RNA, and total protein content after fertilization and early development. However, the platelet is not entirely static because the major 160-kD yolk glycoprotein YP-160 undergoes limited, step-wise proteolytic cleavage during early development. Based on previous studies by us and others, it has been postulated that yolk platelets become acidified during development, leading to the activation of a cathepsin B-like yolk proteinase that is believed to be responsible for the degradation of the major yolk glycoprotein. To investigate this possibility, we studied the effect of addition of chloroquine, which prevents acidification of lysosomes. Consistent with the postulated requirement for acidification, it was found that chloroquine blocked YP-160 breakdown but had no effect on embryonic development. To directly test the possibility that acidification of the yolk platelets over the course of development temporally correlated with YP-160 proteolysis, we added 3-(2,4-dinitroanilo)-3-amino-N-methyldipropylamine (DAMP) to eggs or embryos. This compound localizes to acidic organelles and can be detected in these organelles by EM. The results of these studies revealed that yolk platelets did, in fact, become transiently acidified during development. This acidification occurred at the same time as yolk protein proteolysis, i.e., at 6 h after fertilization (64-cell stage) in Strongylocentrotus purpuratus and at 48 h after fertilization (late gastrula) in L. pictus. Furthermore, the pH value at the point of maximal acidification of the yolk platelets in vivo was equal to the pH optimum of the enzyme measured in vitro, indicating that this acidification is sufficient to activate the enzyme. For both S. purpuratus and Lytechinus pictus, the observed decrease in the pH was approximately 0.8 U, from 7.0 to 6.2. The trypsin inhibitor benzamidine was found to inhibit the yolk proteinase in vivo. By virtue of the fact that this inhibitor was reversible we established that the activity of the yolk proteinase is developmentally regulated even though the enzyme is present throughout the course of development. These findings indicate that acidification of yolk platelets is a developmentally regulated process that is a prerequisite to initiation of the catabolism of the major yolk glycoprotein.

121 DEVELOPMENTAL CHANGES IN THERMOPROTECTIVE ACTIONS OF INSULIN-LIKE GROWTH FACTOR-1 ON THE PREIMPLANTATION BOVINE EMBRYO

2011 ◽  
Vol 23 (1) ◽  
pp. 165
Author(s):  
A. Q. S. Bonilla ◽  
L. J. Oliveira ◽  
M. Ozawa ◽  
E. M. Newsom ◽  
M. C. Lucy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Heat Shock ◽  
Differentially Expressed Genes ◽  
Blastocyst Stage ◽  
Differentially Expressed ◽  
Bovine Embryo ◽  
Blastocyst Development ◽  
Developmentally Regulated ◽  
Cell Embryo

Insulin-like growth factor-1 (IGF1) is an important endocrine signal for regulation of early embryonic development. It increases the proportion of preimplantation embryos becoming blastocysts, alters blastocyst gene expression, improves resistance of embryos to various stresses and can enhance survival of embryos after transfer to recipients. The present study had 2 objectives. The first was to determine whether the thermoprotective actions of IGF1 on the preimplantation bovine embryo were developmentally regulated, with the 2-cell embryo being refractory to IGF1. The second was to determine the molecular basis for the improved competence of embryos treated with IGF1 to establish pregnancy after transfer to heat-stressed recipients. Heat shock at 41°C decreased (P < 0.005) the percentage of 2-cell embryos becoming a blastocyst at day 8 (39.5 v. 21% for 38.5 and 41°C, respectively), and treatment of embryos with 100 ng mL–1 IGF1 did not provide thermoprotection to 2-cell embryos heat shocked at 41°C (21 v. 21% for control and IGF1-treated embryos, respectively). Heat shock at 41°C had no effect on blastocyst development of day 5 embryos. However, exposure to 42°C reduced (P < 0.001) blastocyst development of day 5 embryos (87 v. 47.6% for 38.5 and 42°C, respectively). Furthermore, treatment of embryos with 100 ng mL–1 IGF1 reduced (P = 0.05) the effect of heat shock at 42°C on day 5 embryos (48 v. 66% control and IGF1-treated embryos, respectively). Failure of IGF1 to alter 2-cell embryo survival after heat shock was not associated with reduced expression of genes involved in IGF1 signaling (IGF1R, RAF1, PI3K, and MAPK), as shown by quantitative real-time RT-PCR assay, or in amounts of immunoreactive IGF1R protein. Treatment with IGF1 had little effect on the transcriptome at the blastocyst stage, with a total of 102 differentially expressed genes identified. Among the differentially expressed genes were several involved in apoptosis, protection against free radicals, and development. Changes in gene expression are consistent with IGF1 acting to induce an anti-apoptotic state and inhibit neurulation. In conclusion, thermoprotective actions of IGF1 are developmentally regulated. Failure of IGF1 to protect the 2-cell embryo from heat shock could reflect the fact that these embryos are maximally sensitive to damage caused by heat shock or reflect the quiescence of the embryonic genome at this early stage in development. Changes in gene expression at the blastocyst stage induced by IGF1 could contribute to the increased survival of IGF1-treated embryos when transferred during periods of heat stress. Support: USDA NRI 2007-35203-18070 and 2009-65203-05732.

Activation by Heat Shock of hsp70 Gene Transcription in Sea Urchin Embryos

1995 ◽  
Vol 217 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
G. Sconzo ◽  
M.G. Ferraro ◽  
G. Amore ◽  
G. Giudice ◽  
D. Cascino ◽  
...  
Keyword(s):  
Heat Shock ◽  
Gene Transcription ◽  
Sea Urchin ◽  
Hsp70 Gene ◽  
Sea Urchin Embryos
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