Plasmodesms . They are cytoplasmic connections that cross the cell wall between adjacent cells. Since the protoplasts of living cells are linked together by means of plasmodesms, they constitute a unique syllable.
The movement of substances through plasmodesms is called sympathetic transport. The cell walls, the lumens of the dead cells and the intercellular spaces that surround the syplast, also forming a continuum, are contrasted under the name of apoplast; the movement of substances in it is known as apoplastic transport.
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- 1 Composition
- 1 Primary Plasmodesms
- 2 General structure of plasmodesms
- 3 Scores (pits or alveoli)
- 4 parts
- 1 Bordered or beaded scores
- 5 Possible states of plasmodesms
- 6 Macromolecular traffic
- 7 Macromolecules associated with PD
- 1 Vesicular Traffic Proteins
- 8 Movement through PD
- 9 Perspectives
- 10 Sources
Figure 1 . Diagram of plasmodesmos in transcorte.
Figure 2 . Plasmodesm diagram between two cells.
Plasmodesms are made up of a double membrane: the outer one is the plasma membrane, surrounded by a thin layer of calose , the inner one corresponds to the demotubule, which is a tubule of the endoplasmic reticulum, between the two there is a cytoplasmic sleeve. The components of the internal face of the biomembrane that forms the demotubule fuse with each other, so that the demotubule does not have a lumen. Cell-to-cell transport is limited to the “cytoplasmic sleeve” surrounding the demotubule ( Figure 1 and Figure 2 ).
They are formed during cytokinesis at the same time as the cell wall.In special cases such as grafts, scar tissue, parasite-host interface, secondary plasmodesms are formed in places where they did not exist before or by modification of primary plasmodesms. They do not form in walls that on the other side do not have living cells. When one cell dies, it rapidly thickens the chloose coating in the neighboring cell and plasmodesm is obliterated.
Occasionally plasmodesms branch to one or both sides of the middle lamella; in that case a cavity is formed. They rarely appear scattered in the primary walls, sometimes in which they are quite thick, as in the cells of the endosperm of certain seeds such as those of Diospyros. They are commonly grouped in thin, depressed areas of the primary walls, constituting a primary scoring field. or overriding score. At the limit of the primary scoring field, the microfibrils are arranged in parallel, forming a circle or oval.
General structure of plasmodesms
Plasmodesms ( PD ) are channels that pass through the cell wall joining the cytoplasms of adjacent cells and facilitating intercellular communication. The current model of PD structure suggests the presence of a compressed membranous tube derived from the endoplasmic reticulum ( ER ) that is present in the center of the canal and is called a demmotubule. Globular proteins that are closely associated with transmembrane proteins project like spiral rays from the demotubule to the plasma membrane ( PM ) dividing the cytoplasmic cylinder and forming microchannels. Basically there are two types of PD, which are formed under differential conditions in cell development. The PD primary, formed during cytokinesis in cell plate cells in division. The PD side, are formed post-cytokinesis and can be assembled along the cell wall , allowing an increase in the molecular traffic and / or connection of cells citoquinéticamente unrelated. The PD are primary or secondary and can be simple or branched, provided that generally correlates with maturity and / or tissue function.
Punctures (pits or alveoli)
Figure 3 . Simple scoring diagram
Scores are discontinuities in secondary wall deposition at the level of a primary scoring field, although they can also be differentiated in areas where there were no primary fields. Two main types of scores are distinguished: Simple score The secondary wall is abruptly interrupted. It occurs in parenchymal cells, fibers and sclereids ( Figure 3 ).
Figure 4 . Branched scoring diagram.
The closing membrane or alveolar membrane formed by the middle lamella and thinned primary wall; the scoring cavity formed by the discontinuity in the deposition of the secondary wall, sometimes covered by a warty layer. If the secondary wall is very thick, the cavity forms the scoring channel, which runs from the lumen to the closing membrane. As the size of the lumen decreases with increasing wall thickness, the channels of two or more neighboring scores can be merged, thus constituting the so-called branched scores ( Figure 4 ).
Bordered or beaded scores
They are those in which the secondary wall, when deposited, makes a rim or areola forming the scoring chamber that opens to the cellular lumen through the scoring opening. The shape of the latter may or may not agree with the contour of the areola. They are more complex and varied in structure than the simple ones. They mainly appear in fibrotracheids and xylem conductive elements ( Figure 5When the secondary wall is very thick, it is possible to differentiate in addition to the chamber, the scoring channel, with the internal opening towards the cell lumen, and the external opening towards the scoring chamber. The channel may have a flattened funnel shape, and so the internal and external openings differ: the internal is lenticular or linear and the external is small and circular. In a couple of scores, the internal openings are often cross-arranged, relative to the slanting arrangement of the cellulose fibrils on the secondary wall ( Figure 6 ).
Possible states of plasmodesms
Generally, the function of PDs is characterized by the plasmodesmal exclusion limit size ( TLE ) of molecules that move passively. The PD can occur in three states: open , closed and dilated . The PD closed, are characterized by lack of exchange of molecules between cells neighboring and such a state may be transient or permanent, involving total or partial disassembly of the cell wall PD. The open state, whose TLE depends on the cell type in question and its physiological status, is characterized by the free movement of ions, metabolites and growth regulators. Finally, an extension of the open PDs , the dilated PDs, allow the movement of macromolecules ( MC ) that exceed the TLE given for the tissue in question. The dynamics between the different states can be explained, in part, thanks to the actinamiosin complex that is arranged helically along the demotubule connecting the MP with it, this actinamiosin complex could act in concert with proteins associated with calcium such as centrin (protein which works by contracting in response to increases in cytoplasmic Ca2 + concentration and relaxes via ATP- mediated phosphorylation) and with calreticulin (a highly conserved calcium sequestering protein) modulating the size of the cytoplasmic ring and microchannels via Ca2 + sensitive pathways . Reinforcing the previous idea, it has been shown that transient elevations in the cytoplasmic Ca2 + concentration result in a transient closure of the plasmodesms of vascular plants.
Recently, two cell-to-cell macromolecule trafficking models have been proposed that involve opening and closing PDs. These models are based on specific proteins that interact directly or indirectly with PDs, modulating their state (Lucas and Lee, 2004). In the first model, the ‘gate’ model, the microchannels dilate due to the union of a protein called gate open (GO) with its respective plasmodesmal gate receptor, in this way, molecules that can move freely through the cytoplasm and spread to neighboring cells. Partial or total closure of the microchannels, depending on the physiological status and tissue involved, occurs by removal of GO through direct interaction with a protein called gate closure (GC). In the second model, the selective movement of macromolecules, transporter proteins and / or chaperones deliver the charge (ribonucleoprotein complexes or proteins) to an anchor protein found in PDs; in this way, the protein interaction induces dilation of the microchannels, followed by selective traffic of the charge to neighboring cells. During this process, small molecules can co-diffuse through the dilated channels. Microchannel closure occurs by removal of the carrier protein from the small molecules can co-diffuse through the dilated channels. Microchannel closure occurs by removal of the carrier protein from the small molecules can co-diffuse through the dilated channels. Microchannel closure occurs by removal of the carrier protein from theanchor protein . Together, proteins specialized in the opening and closing dynamics of PDs and constituent proteins of PDs such as actin, myosin VIII, centrin and calreticulin effectively modulate and regulate the traffic of molecules and MC from cell to cell.
Macromolecules associated with PD
Several MCs associated with the PDs have been identified. For this reason, several studies have examined the interaction between viral movement proteins (PMV) and endogenous plant proteins, in order to identify host factors involved in MC traffic to PD. With few exceptions, plant proteins that interact with PDs can be grouped into different categories. Chaperones. Several transport proteins have been shown to interact directly with DNAJ-type chaperones, which have a wide range of functions including, importing proteins into organelles and regulation of other chaperones such as HSP70, which in turn play an important role in conformational change and trafficking of certain proteins before passing through the PD. Many chaperones bind directly to molecular motors, thereby ensuring delivery of the MC to the cytoskeleton. Several molecular motors including those from the myosin, kinesin, and dynein families have been seen to interact with cellular proteins that determine specificity in cell transport.
Vesicular Traffic Proteins
Vesicular traffic proteins. Rab GTPases proteins that have a dual function, specificity to bind to the molecule to transport and ability to bind said load to the cytoskeleton, are attractive candidates in mediating MC trafficking. In all eukaryotes, Rab plays an important role in determining specialized vesicle trafficking. There are a large number of proteins in and around PDs which suggests that many of these proteins are directed to PDs via pathways that involve the use of vesicles and transport of them mediated by Rab proteins. In the case of viruses, a way by which they could effectively reach the PDs for their subsequent systemic infection,
Movement through PD
In the most widely accepted current model for selective MC traffic, the cytoskeletal motor, and not the load, is phosphorylated to allow MC traffic through the pore. In this way, a protein would be required to transport the MC to the cytoplasm. Once there, the MC would associate with a chaperone, which in turn binds the charge to an appropriate molecular motor. The continuity of the actin cytoskeleton from the cytoplasm to the PD provides a path for directional traffic from the MC to the PD. Once in the PD, an anchor protein binds the MC either by direct binding or alternatively by binding to the myosin motor in its C-terminal domain. The conformational opening motif present in the MC activates the myosin-specific kinase that phosphorylates it, resulting in the release of myosin from the membrane and a concomitant increase in PD TLE. The MC is thus transported to the adjacent cell via the myosin motor domain through the actin filaments that pass through the PD. In this model, cycles of phosphorylation and dephosphorylation of the molecular motor regulate the binding and detachment of the MC from the MP that covers the PD, allowing a generic mechanism for regulating the opening of the PD.
Although knowledge about plasmodesms has advanced, there are still unresolved questions. How is the formation of these structures in a mature cell? How is the exquisite regulation of molecules between the phloem and the accompanying cells accomplished? What other molecules are involved in opening, closing, and transporting through plasmodesms? These and other questions that remain unsatisfactory in a satisfactory way should be topics to be addressed in future research.