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Vol. 16—1962 - NorthEastern Weed Science Society

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a copious precipitate deposits after ten minutes of boiling. Subsequent<br />

experiments have revealed that this effect is proportional to the concentration<br />

of 2,4...D employed, both in stElllla, where 2,4-D promotes growth, and in<br />

roots, where 2,4-D inhibits growth. The minimal effective concentration<br />

appears to be about 10-6 molar in both tissues and the effect rises linearly<br />

with the logarithm of the conoen~rat1on emplqyed. There is no evidence of<br />

an optimum. Certain of these facts have, of course,. compelled us to doubt<br />

the physiological significance of this phenomenon, for, as you are aware,<br />

a graph relating growth effect to concentration of auxins applied to plant<br />

tissues usually shows a sharp optimum concentration, for growth promotion.<br />

I believe, however, that this is not a serious stumbling block, for in our<br />

laboratory we have obtained evidence that the growth inhibitional phase of<br />

auxin action on stems, at least, is quite separable from the grolvth promotional<br />

phase •. For example, in experiments with excised pieces of etiolated<br />

pea stem, it can readily be shown that when sugar is added to the medium<br />

there is an auxin optimum, but when sugar is omitted from the mediumthere<br />

is no auxin optimum. Regarding the lack of difforential effect on root<br />

and stem in our protein test system as contrasted with differential effects<br />

of auxin on root and short in vivo, we need only remark that there is good<br />

evidence to believe that the basic action of auxin in all tissues is fundamentally<br />

the same. Whether one aohieves growth promotion or growth inhibition<br />

as a result of auxin application is probably the result of secondary<br />

reactions of various types in the different tissues. At any rate, we do<br />

not believe, at the moment, that we need to relegate the results we have<br />

found to the limbo of the physiologically meaningless.<br />

What evidenoe do we have that the phenomenawe have discovered are<br />

in fact biologically meaningfUl? In the first place, the effect appears to<br />

be elicited only by those t,ypes of molecules which show auxin activity.<br />

For example 2,4-D and indoleacetio aoid are most active, phenylacetic<br />

acid and.2-3-5-triiodobenzoic acid are moderately active, and the antiauxin<br />

p-chlorophenaxyisobut,yTic acid is cqinpletely inactive. Secondly, only<br />

those cells of both etiolated and green pea plants which are capable of<br />

responding to auxin from a growth point of view show the altered coagulability<br />

pattern of proteins. Thirdly, kinetic studies have convinced us<br />

that altered heat coagulability maymnnifest itself as soon as two hours<br />

after application of auxin, although the usual time lag is four hours.<br />

Since we can first detect growth differences between .control and treated<br />

tissues in about one hour or so we are at least close to the range in which<br />

our effect must operate to be of significance in the control of growth.<br />

Fourthly, gibberellin, which produces no marked effect on the growth of<br />

excised pea stem tissue, is also without effect on alteration of the heat<br />

coagulability of proteins, though it does appear to synergize slightly with<br />

auxin, as it does in growth itself.<br />

an'the·chemicalside we have also done certain experiments to try to<br />

understand the nature of changes wrought in the proteins. The first question<br />

would appear to be this1 Is it protein itself which is changed by auxin<br />

trea"bnent or can we possibly be altering something else in the tissue which<br />

results in an altered stability of the proteins toward heat? The first<br />

thing to remark here is that the altered coagulability persists after prolonged<br />

31

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