The polymer-trapping hypothesis functions in some species of plants and involves symplastic phloem loading. According to this hypothesis, mono- and di-saccharides are small enough to be capable of diffusing from mesophyll cells into companion cells along a concentration gradient through plasmodesmata.
In the companion cells these simple sugars are combined into larger oligomers, oligomers of sufficient size to prevent their diffusion back through the narrow plasmadesmata leading into the mesophyll cells. However, due to the large diameter of the branch plasmadesmata leading into the sieve element from the companion cell, these sugars can diffuse into the sieve tube and be transported.
In contrast to the symplastic route, some species have no plasmodesmatal connection between the mesophyll cells and the companion cells. There is direct evidence for phloem loading from an apoplastic pathway involving a proton pump AHA3 , and a proton-sucrose symporter SUC2 , located in the companion cells. Sucrose, produced by the mesophyll cells is dumped into the apoplast and then recovered into the companion cells via SUC2. Regardless of which pathway is used, companion cells are implicated in the delivery of material to the sieve elements.
However, recent evidence has led to the belief that a second apoplastic loading mechanism exists in the sieve elements themselves. Immunolocalization experiments have demonstrated the presence of a proton-sucrose symporter SUT1 in the plasma membrane of the phloem sieve element. The organelles must therefore, be anchored in place along the cell periphery. Additionally, any intra-phloem transport of molecules not abundant in the translocation stream must be compartmentalized, probably within the lumen of the sieve element reticulum SER.
Sieve elements develop hydrostatic pressures in excess of 30 atmospheres! The cell walls of sieve elements are therefore, modified to be able to contain this high pressure without bursting. One of the most fundamental modifications is the production of cellulose microfibrils at right angles to the axis of elongation of developing sieve elements. These microfibrils act like hoops around a barrel, assisting the cell to maintain its shape under the pressures developed within.
Along with the obvious practical advantage of not bursting, this reinforced cell will not undergo deformation bulging although considerable pressure is applied within, thereby propagating this pressure longitudinally along the phloem tissue. Hormonal control of xylogenesis:. Endogenous auxin appears to be responsible for determining the initiation of tracheary element TE differentiation and the size of the resulting TEs.
Cytokinin, apart from enhancing the sensitivity of tracheary initials to auxin, is also required for the induction of TE differentiation and its progression to completion. There is indirect evidence that ethylene is also involved in controlling TE development. Recently, brassinosteroids have been shown to be necessary for the transition from stage II to stage III of tracheary element differentiation see below. As mentioned above, much of what is known about xylem differentiation at the molecular level has been acquired using the inducible Zinnia elegans cell culture system.
This system induces parenchymal cells in culture to first de-differentiate and then to re-differentiate into TEs transdifferentiation. The molecular markers identified in this system reflect its artificial nature in that the de-differentiation phase is not usually present in normal TE differentiation from protoxylem or cambial tissue. Hence the system has more in common with wound-induced TE differentiation where pre-existing cells undergo de-differentiation prior to developing into TEs.
Stage I: De-differentiation:. Using the Zinnia mesophyll cell as a model, this stage commences with the cells losing the ability to conduct photosynthesis, the expression of wound-induced genes and the acquisition of the ability to elongate and differentiate. Three groups of genes are up-regulated during this stage, 1 wound-induced genes; 2 genes whose products are associated with the protein synthetic apparatus and; 3 the remainder.
Stage II: Restriction of developmental potential:. The accumulation of TED2, 3, and 4 Tracheary element differentiation-related genes gene products. This accumulation occurs between 12 and 24 hours prior to the synthesis of the secondary cell wall. These same inhibitors also repressed the expression of all TEDs. There is a marked increase in the transcript abundance of a number of genes whose products are involved in the protein translational machinery which is correlated with a dramatic increase in protein and RNA amounts present in these differentiating cells.
Additionally, tubulin gene expression increases, providing the means of orchestrating secondary cell wall synthesis in the third stage of development.
Actin gene transcription increases as well, and large cables of actin form along which cytoplasmic streaming occurs. Brassinosteroids are necessary for the transition from stage II to stage III of tracheary differentiation. In this last stage of tracheary element differentiation the secondary cell wall, necessary for the structural strength required to withstand the high negative pressures exerted by transpiration without implosion, is synthesized.
The secondarily thickening of the cell wall occurs by the synthesis of cellulose microfibrils perpendicular to the direction of flow which, as in phloem, strengthen the element like hoops around a barrel. Additional structural support is provided by cell wall proteins. An extensin protein as well as an arabinogalactan protein are in high concentration in mature tracheary elements.
A characteristic alteration to the cell wall of the tracheary elements at this stage is their heavy lignification. Programmed cell death see below is tightly coupled temporally with secondary cell wall thickening in this stage of xylogenesis. Finally, autolysis occurs culminating in the generation of a cell corpse…a mature xylem element.
Apoptosis Programmed cell death PCD vs necrosis:. All cells die. How they do so varies. Some are slated for death internally, genetically programmed to die a physiological death while others die due to injury. Apoptosis or programmed cell death , is a process of death from internal factors up-regulated in some cells during normal cellular differentiation and development of multicellular organisms. This process is also involved in tissue homeostasis, pathological conditions and aging.
Cells undergoing apoptosis are characterized by cell volume loss, plasma membrane blebbing, nuclear condensation, and endonucleolytic degradation of DNA at discrete intervals. Not all cells die through apoptosis. Dramatically traumatized cells such as those suffering sever wounding or other overwhelming stress undergo necrosis , a non-physiological death involving cell swelling, eventual lysis, and the leakage of the cell contents into the intercellular space.
Necrosis does not usually play a role in differentiation and development and so will not be dealt with further. Vegetative development: Vascular tissue differentiation: Just prior to the completion of seed germination, the provascular tissue in the embryo differentiates into protoxylem and protophloem, providing the rudiments of a vascular system until more permanent metaxylem and metaphloem differentiate.
Vascular pattern ontogeny: Provascular tissue and the ground meristem are both derived from the uniformly meristematic tissue of the leaf primordium and only differentiate upon the commencement of cell division and expansion associated with leaf development.
Dicot: The vasculature of dicots develops through three major phases during leaf morphogenisis and growth. This group includes some early diverging angiosperms ANA grade families and magnoliids , but the large majority of these occupy a single clade called the eudicots. In addition to developmental features, there are a few morphological and anatomical traits you can use to distinguish between these two major groups.
Monocots do not have true secondary growth, though some such as bamboo form tough, woody stems. Learning Objectives Compare and contrast monocots and eudicots. Differentiate between monocot and eudicot flowers and leaves. Monocot and Dicot Roots. Monocot and Dicot Stems. Monocot Glossary. Dicot Glossary. When you select "Subscribe" you will start receiving our email newsletter.
Use the links at the bottom of any email to manage the type of emails you receive or to unsubscribe. See our privacy policy for additional details. Learn Site. Monocot and dicot leaves contain similar types of dermal, ground, and vascular tissues, but they are arranged differently within each type of leaf.
Leaf dermal tissue Both monocot and dicot leaves have an outer, waxy layer called the cuticle that covers the dermal tissue of the upper and lower epidermis. Leaf vascular tissue In monocot and dicot leaves, vascular bundles are surrounded by one or more layers of parenchyma cells known as bundle sheaths.
Monocot leaves have stomata on the upper and lower sides of the leaf, and their veins run parallel to one another. Dicot leaves have stomata on the lower side of the leaf. They also have net-like veins and two types of mesophyll. Visible Body Biology Learn more. External Sources A microscope slide of a grass leaf with a description of bulliform cells from UTexas. Get our awesome anatomy emails! About News Contact. All Rights Reserved. User Agreement Privacy Permissions.
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