Why do Vegetative Shoot Apical Meristem Cells possess
Reticulate Mitochondria?
The fact that reticulate mitochondria are found in shoot (SAM)
but not in root apical meristem cells suggests that a reticulate
mitochondrial system is not essential to accomplish cell division
in plants. This leads us to ask what features distinguish SAM from
root apical meristem cells and from the non-dividing cell types that
contain small, oval or sausage-shaped mitochondria? The function
of SAM cells is to produce the aerial parts of plants, including
leaves and flowers. Interestingly, with the exception of the young LP
meristematic cells, all of the cell types generated by SAM cells such as
differentiated leaf and floral organ cells, possess small, conventional
mitochondria. Thus, it appears that the capability to form reticulate
mitochondria is specific to vegetative SAM, and is progressively lost
as the derived meristematic cells become physically displaced from
the vegetative SAM region and adopt their primary function. This
loss even seems to occur during the vegetative-to-floral meristem
transition, given its absence in flower cells.
Considering this temporal and spatial confinement of cell
types with reticulated mitochondria,1 we conceive mitochondrial
reticulation as a mechanism to allow for an efficient homogenization
of the mitochondrial content, including mitochondrial DNA
(mtDNA) and mtDNA products, during the vegetative growth
of the SAM. It can be argued that other mechanisms, such as the
elevated frequencies of transient fusion and fission reported for
small, oval mitochondria in other cell types,15 could also account for
the elevated rate of recombination that defines the plant mtDNA.12
However, this mechanism does not guarantee an equal distribution
of the mtDNA after fission.15 We rather believe that the permanent
presence of a significantly larger, common space may expedite the
process of nucleoid encounter and thus make recombination more
efficient. Furthermore, not only mtDNA recombination can be positively
affected by the presence of a permanent, large mitochondrion
to fuse with and to divide from. This larger space has the potential
to act as a pool of mitochondrial components that small, individual
units may use to homogenize their protein content, prevent the
accumulation of undesired mutations, and minimize the chances of
containing no mtDNA. Additionally, it is also a means to ensure an
equal partitioning of the chondriome between daughter cells during
cytokinesis.
The presence of this improved mechanism for homogenization
of mitochondrial distribution and contents appears essential in