5
Influence of Source Strength on Leaf
Developmental Programming
Steven Rodermel and Martin Spalding
Iowa State University, Ames, Iowa
Adam Miller
Lorain County Community College, Elyria, Ohio
117I. INTRODUCTION
Dicot leaf ontogeny is a complex process that is regulated by a variety of exogenous factors (e.g., light)
and endogenous factors (e.g., hormones, developmental signals) [1,2]. Striking alterations occur in pho-
tosynthetic rates during leaf development, and these changes have been used to monitor the progression
of this process. In general, increasing photosynthetic rates are coincident with leaf expansion; a phase of
maximal rates occurs at full expansion; and finally, a prolonged senescence phase of declining rates takes
place in the fully expanded leaf [3]. The senescence phase is marked by a progressive yellowing of the
leaf, loss of protein (most notably of Rubisco), and the translocation of resources to growing parts of the
plant [4–8].
The changes that occur in photosynthetic rates during leaf ontogeny are reflected in marked changes
in plastid form and function. During leaf expansion, chloroplasts develop from undifferentiated proplas-
tids in the apical meristem and undergo a series of rapid divisions to form mature organelles [9]. Once full
expansion is attained, chloroplasts differentiate into “gerontoplasts.” This differentiation process com-
prises a progressive loss of pigments and organized lamellar structures and an accumulation of lipid-con-
taining plastoglobuli [8]. Because most multimeric protein complexes in plastids are composed of sub-
units encoded by genes in the nucleus and the organelle [10], a central element of leaf developmental
programming involves the integration and coordination of gene expression in the nuclear-cytosolic and
chloroplast genetic compartments. The mechanisms are poorly understood.
A. Carbohydrates and Leaf Development
It has been suggested that carbohydrates play a central role in regulating leaf development [11–15]. Ac-
cording to the “sink regulation of photosynthesis” hypothesis, a decrease in sink demand leads to a
buildup of carbohydrates and an inhibition of photosynthesis in source leaves [16–18]. In some cases this
inhibition occurs as a consequence of decreases in photosynthetic gene expression at the level of tran-
scription [14,16,18–24]. We and others have extended this hypothesis to leaf development and have sug-
gested that feedback inhibition of photosynthetic gene expression by carbohydrates is an important fac-
tor that regulates the initiation of the senescent decline in photosynthesis [12,15,25–28]. General support
for this notion comes from studies showing that plants grown in elevated light intensities have enhanced