compensation point and senescence?

Mark E. Kubiske mkubiske at
Mon Nov 17 16:11:15 EST 1997


Much of this issue has to do with vacular connections within and between
plant modules.  For example, the phylotactic arrangement of leaves on a
cottonwood stem are not all vascularly connected.  Developing cottonwood
leaves that are CHO sinks receive CHO from sources at very specific
positions (3, 5 and 6 I think, counting down from the apex).  See the work
by Dickson, Isebrands et al.

A good example lies with reproductive structures (seeds) that are very
large C sinks.  Developing seeds on reproductive shoots do not import 14C
from purely vegetative adjacent shoots.  Current or newly fixed
photosynthate seems to be immediately utilized with the module (structures
that originated from a single meristem), or stored.  An exception is with
CHO storage --  as C is mobilized from storage tissues, does it translocate
to a predictable sink?  Perhaps this is the issue with  the  clonal/ramet
C-sharing example you raised.   A similar example is with managed pine
plantations.  Stumps remaining after thinnings may remain alive via root
grafts with still-standing trees.

As far as shade-induced C imbalance and leaf senescence,   I agree with
Janice that shaded leaves do eventually simply "starve".  No doubt there is
some threshold at which leaves are no longer to mobilize, as you say, every
last bit of "suitable and available carbohydrate and lipid in the leaf
until they are all gone ".  Also, I'm not sure how this differs from what
you call "normal" senescence in which photosynthetic machinery shuts down
and leaves senesce.  At the risk of getting too teleolgical, we can at
least speculate as to what would happen if shaded leaves did in fact become
CHO sinks and parasitize the rest of the tree.   As the tree grew in height
and self shading occupied a greater and greater proportion of the crown,
the tree (rather than the leaf) would quickly reach a zero C-balance point
and fail go grow.  As it is, tree growth is accompanied by a decrease in
the proportion of C fixing to C respiring biomass.  The problem would be
compounded by retention of non-productive, N-rich, rapidly respiring leaves.

Dr. Mark E. Kubiske                     Phone: 601-325-3550
Department of Forestry            Fax:   601-325-8726
Box 9681                                   Email: mkubiske at
Mississippi State University
Mississippi State, MS  39762-9681

>Ahh yes I see the source of the confusion--I was thinking more about the
>light compensation point when a shaded leaf is no longer a net source of C
>to the plant. ...a hastily written note.  However the CO2 compensation
>point is still relevant.
>The interest for us is on the role of resource supply on leaf longevity and
>senescence.  What does starvation mean in a leaf?  High-light leaves have
>shorter lifespans compared to low-light leaves.  Likewise, in some studies
>it has been shown that leaves on plants grown under CO2 enrichment senesce
>early.  This is consistent with various theories on the relationship
>between metabolism and senescence for unitary (i.e. non-modular and
>non-clonal) animal systems.  Thus there is a theoretical basis to the
>observation that reduced caloric intake can extend life in animals.  If
>leaves are put in the dark they quickly die.  However, dark induced loss of
>function in leaves does not appear to be the same as "normal" senescence.
>This isn't too surprising really.  (And likewise keeping all food and water
>from an animal will NOT extend its life!) But what happens to leaves under
>very low light (i.e., below the light compensation point)?  Or very low
>CO2?  The text book explanantion is that they just starve to death.  Is
>this true?  Does the leaf start respiring away every suitable and available
>carbohydrate and lipid in the leaf until they are all gone?  Is there any
>conservation of respiratory substrate for the generation of energy for use
>in leaf functions other than C assimialation?  Clonal plants can share
>resources. Shading an older ramet while leaving a new daughter ramet in
>full sun can reverse the source/sink polarity so that the older ramet
>acquires C from the dauhter ramet.  Why doesn't the same thing happen in
>leaves?  Or are the textbooks wrong?  Do "starving" leaves still breakdown
>in an orderly and regulated way allowing remobilization and export of
>nutrients for use in other parts of the plant?  Can "starving" leaves send
>hormone or hoirmone-like signals to other parts of the plant in the event
>of insect or pathogen attack?  Can "starving" leaves turn on genes and
>upregulate enzymes necessary for these regulated processes?
>At  5:27 PM 11/13/97 -0500, Janice M. Glime wrote:
>>If a plant is in a situation where CO2 concentration is below the CO2
>>compensation point, it means the plant will use more CO2 in respiration
>>that it will fix in photosynthesis.  Yes, in a sense it does starve.  I am
>>having difficulty interpreting your question about becoming a sink.  If it
>>has too little CO2, how could it become a sink for CO2?
>Reduced carbon--not CO2.
>  Help me out with
>>your thinking here - perhaps I can help a little more.
>> >
>>> Here's a question Doug Bielenberg and I have been pondering that might
>>> be interesting for the group to consider:
>>> What is the mechanism by which a plant recognizes that a leaf is below
>>> the CO2 compensation point?  This is often used to explain why shaded
>>> leaves begin to senesce.  Why doesn't the leaf just become a sink for
>>> carbon?  It doesn't just starve does it?  If the CO2 compensation point
>>> or a negative carbon budget is the cue for leaf senescence what is the
>>> mechanism?  It may be pertinent to recall that leaves can have functions
>>> other than just carboon acquisition; e.g. nutrient stores used for
>>> growth elsewhere in the plant, transpirational "sinks" driving nutrient
>>> uptake, modifiers of canopy microclimate, etc. etc.
>>> Any ideas on this topic?
>>> John Skillman
>John Skillman
>209 Buckhout Laboratory
>Pennsylvania State University
>University Park, PA 16802
>Tel: 814-863-7399
>FAX: 814-863-7217
>email: jbs11 at

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