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Discussion des communications de J. Kruh, R. Williamson et G. Schapira
606
DIscUSSION.
DISCUSSION
d e s c o m m u n i c a t i o n s de J . K R U H , e t G. S C H A P I R A .
R. WILLIAMSON
R. W I , L L I A M S O N : Can I come in with some experiments on m i x e d systems w h i c h have given the same sort of results as H e y w o o d ' s ? Mathews at Cambridge obtained mouse hemoglobin biosynthesis by adding m R N A of a mouse hemoglobin to ribosomes from mouse ascitic cancerous cells. G. S C t t A P I R A : W e have also f o u n d that there is no KCI factor specificity for reticulocytes in a cell-free system. R. W [ L L I A M S O N : I n the m a m m a l i a n systems, there m u s t be a ribosome binding site of some sort or another w h i c h is not involved in coding. N o w certainly there are regulatory sequences w h i c h exist adjacent to m R N A . A careful examination of the relationship b e t w e e n precursor, beterogenous RNA and the messenger should make the situation clearer. P. M A R K S : D r . Williamson, you m e n t i o n e d in your talk that it is n o w apparent that the defect in lhalassemia is in the non-coding portion of the m R N A . W h a t is the evidence for that ? R. W I L L I A M S O N : There are two possibilities : either the messenger is abnormal, possibly in its non-coding portion, or there is a decrease in the total amount of messenger.
P. M~RKS : F r o m our data I don't t h i n k w e would be willing to distinguish between a defect in the amount of messenger or in its quality. D. J. W E A T H E R A L L : The translation time as measured by Dintzis's technique in palients with ~ thaIassemia, and more recently we have measured also the translation time of the a chain in patients w i t h haemoglobin H disease, appears to be normal. So this would suggest lhat probably the defect is either in the total amount of messenger, or in the rate of initiation. R. W I D L I A ~ S O N : It m i g h t be true that ribosomes f r o m different cells have a different coding spectrum. The whole question of regulation through the ribosome proteins and its significance is so great that I t h i n k that it is necessary to be absolutely sure that contaminants are not responsible for the differences observed between ribosomal proteins within the same species. G. SCH/kPSRA : I consider we have an indirect evidence. W h e n we compare the protein composition of ribosomes from a normal rat liver and from a hepatoma in the same species, we have exactly the same pattern. It is not a direct demonstration, but it is a good indication.
BIOCHIMIE, 1972, 54, n ° 5 - 6 .
DIscUSSION.
DISCUSSION
d e s c o m m u n i c a t i o n s de J . K R U H , e t G. S C H A P I R A .
R. WILLIAMSON
R. W I , L L I A M S O N : Can I come in with some experiments on m i x e d systems w h i c h have given the same sort of results as H e y w o o d ' s ? Mathews at Cambridge obtained mouse hemoglobin biosynthesis by adding m R N A of a mouse hemoglobin to ribosomes from mouse ascitic cancerous cells. G. S C t t A P I R A : W e have also f o u n d that there is no KCI factor specificity for reticulocytes in a cell-free system. R. W [ L L I A M S O N : I n the m a m m a l i a n systems, there m u s t be a ribosome binding site of some sort or another w h i c h is not involved in coding. N o w certainly there are regulatory sequences w h i c h exist adjacent to m R N A . A careful examination of the relationship b e t w e e n precursor, beterogenous RNA and the messenger should make the situation clearer. P. M A R K S : D r . Williamson, you m e n t i o n e d in your talk that it is n o w apparent that the defect in lhalassemia is in the non-coding portion of the m R N A . W h a t is the evidence for that ? R. W I L L I A M S O N : There are two possibilities : either the messenger is abnormal, possibly in its non-coding portion, or there is a decrease in the total amount of messenger.
P. M~RKS : F r o m our data I don't t h i n k w e would be willing to distinguish between a defect in the amount of messenger or in its quality. D. J. W E A T H E R A L L : The translation time as measured by Dintzis's technique in palients with ~ thaIassemia, and more recently we have measured also the translation time of the a chain in patients w i t h haemoglobin H disease, appears to be normal. So this would suggest lhat probably the defect is either in the total amount of messenger, or in the rate of initiation. R. W I D L I A ~ S O N : It m i g h t be true that ribosomes f r o m different cells have a different coding spectrum. The whole question of regulation through the ribosome proteins and its significance is so great that I t h i n k that it is necessary to be absolutely sure that contaminants are not responsible for the differences observed between ribosomal proteins within the same species. G. SCH/kPSRA : I consider we have an indirect evidence. W h e n we compare the protein composition of ribosomes from a normal rat liver and from a hepatoma in the same species, we have exactly the same pattern. It is not a direct demonstration, but it is a good indication.
BIOCHIMIE, 1972, 54, n ° 5 - 6 .