THE CAUSES OF FLUCrUATIONS IN TURGESCENCE
by the nature and amount of the products to wliicli its osmotic properties are due.
Whoro tlie fonner arc unstable, the cessation or alteration of protoplasmic activity will
at once give rise to corresponding changes in the degree of turgidity; where they are
stable and present in considerable quantity, turgidity may remain for long, inappreciably
uiïectcd by death or even complete absence of protoplasm. So long as the osmotic
materials Avlncli are the direct cause of turgescence are present, the latter will persist
under condhious of sufficient water-supply, &c., whether protoplasm be present or absent,
and no action of living pi'otoplasts, unless affecting the stock of osmotic materials, can
produce any effect on the turgescence of cells.
I t may perhaps have been observed that the statement in regard to the effects of
tiirgcscence on tissues is a qualified one. The qualification is necessary, because it does
not invariably happen that turgescence of the protoplasts of a tissue implies turgescence
of the latter as a whole. So long as any protoplast retains its \-itaIity, so long as it
continues to exercise its functional activities, it appears normally to be more or less
turgid, and the coincidence of protoplastic and cellular turgescence, which we find
constantly prevailing in most tissues, is due to the relation which the protoplasts
bear to the cell-cavities within which they are situated, and to the fact tliat even
minimal normal turgescence in the former implies a certain amount of active internal
pressure in the latter. In any case turgescence is dus to the presence of certain
products of protoplasmic activity, but so long as they are confined to the interior of
the protoplasm, cither diiiusedly or within accumulations of cell-sap, and the protoplasts
are situated within cavities with rigid Ti-'alis, it is clear that various degrees of
protoplastic turgescence may be present without any coincident turgescence of the cells
as a whole, and that depression of protoplastic turgescence below a certain degree
must give rise to phenomena of natural plasmolysis. The fall in turgescence in the
protoplasts implies a coiTesponding diminutioi . in their bulk, and as the cell-walls are rigid
this must tend to a separation of the protoplasm from them. In such cases we have
plasmolytic phenomena arising from intrinsic causes, whilst in experimental plasmolysis
they are due to extrinsic ones; in. artificial plasmolysis the exosmotic property of the
medium is raised; in natural plasmolysis the endosmotie properties of the protoplasts
are lowered.
I n the great majority of cases, however, no such phenomena present themselves
under normal circumstances, and even minimal protoplastic tm-gescence implies a certain
degree of turgescence of the tissue as a whole. Tiie interior of the cell-walls is thus
constantly subjected to a certain amount of pressure, which may or may not be accompanied
by correspondingly active distention of the cell-caxities. The actual degree
of tension present at different times, however, varies greatly, the variations being determined
by two perfectly distinct sets of factors—factors telling on the absorptive and
retentive propei-ties of the cell contents, and factors affccting the supply of water
available for absorption and retention, or causing variations in the conditions of external
pressure to wldch the ceUs are exposed. The former are directly related to tlie
functional activities of the protoplasts ; the latter to the general loss and supply of fluid
dependent on atmospheric and telluric conditions, to conditions affecting the waterconducting
elements of the tissues, or to conditions determining local alterations in
pressm-e in the absorptive tissues themselves.
According to the relations which these two sets of factors bear to one another at
different times, variations in the degi'ce of turgescence of the tissues must necessarily be
IN THE MOTOR ORGANS OF LEiVES, S
established. Where conditions favouring the formation of endosmotie products by the
protoplasts are present comcidently with conditions implying abundant general supply and
small general loss, and in tlie absence of any spocml causes ioi- active local filtration,
turgescence will naturally attain its maximum ; wliere active formation of endosmotie
materials coincides witli eoTrditions causing deficient supply or excessive loss of fluid tlie
result in any individual case will be determined by the degree to which each of the
opposed sets of factors happens to prevail ; and, whore a small formation of endosmotie
materials and conditions favouring loss or obstructing supply of fiiiid oceur- coineidently
minimal degrees of turgescence will naturally present themselves.
The variations in turgescence due to the interaction of these various factors must
necessarily give rise to various ultimate results according to the nature of the tissue
in which they occm-. In the eases of tissues in which the conditions for the occm-renco
of natural plasmolysis occur, varying degrees of contact or separation between the
protoplasts and the cell-walls will be present, which may be accompanied by conspicuous
alterations in eolom-, especially where the protoplasts include coloured contents. In other
eases varying degrees of intracellular pressure will constantly prevail which may or
may not be accompanied by corresponding variations in bulk of the tissue. Where the
cell-walls are rigid, either mtrinsically or from their relations to neighbouring parts
variations in intracellular pressm-e alone will be present ; where they are extensile and free
to extend, variations in size wih accompany this. It is only in the latter case that variations
in degree of tnrgidity ean give rise to conspieuoas massive movements, and it does
net, of course, follow that such should mvariably present tlieuiselves even under such
conditions. Variations in the size of the constituent elements of a tissue may result in
mere general increase or decrease of its bulk, and it is only where variations in turgidity
affect opposed masses of tissue in unlike degr""
them.
Mere variations in protoplastic turgidity, may give rise to very conspieuous c „
in the colour- of masses of tissue; variations in the turgidity of the tissue elements"m
a whole, in cases where the cell-walls are rigid, may cause appreciable variation in consistence,
but cannot serve to induce appreciable variations in bulk or i
variations in turgidity of entire tissues with extensile and i
variations in bulk which may or may not be accompanied by conspicuous movomeuls
according to their distribution.
Fluctuations in turgidity are then, under certain circumstancBs, efficient in givinorise
to massive movements in vegetable organisms, and may themselves be caused either
by variations in the natm-e and amount of the products of protoplastic activity, or in
conditions of supply and loss of fluid ; and the question next arises, are they the only
efficient agents in producing this result, or may the active exercise of contractile function
not bo one also, as, according to ordinarily accepted opinion, it may actually be ?
i protoplasts are concerned, it is readily conceivable that active contraction
rations in turgescence, and therefore in bulk, by causiiM the
discharge of fluids included within their substance; but the question which we have to
deal with is, how far is mere protoplastic contraction likely to be efficient in givhrg riso
to alterations m the tin-gescence of cells? In considering this we have in the first nla,
to bear in mind that, in so far as the active protoplasm is concerned, we have uneouivoeal
evidence that contraction does not imply any appreciable alteration in bulk but me,..
change m form, and that therefore contraction of a protoplast situated within a cell cavity
AMI. Eov. Eor. GAUD. C j i c u m Tor. VI.
I that massive movements will accompany
live movements;
cell-walls will cause
So far
y determine