scholarly journals Cell death and cell protection genes determine the fate of pistils in maize

Development ◽  
1999 ◽  
Vol 126 (3) ◽  
pp. 435-441
Author(s):  
A. Calderon-Urrea ◽  
S.L. Dellaporta

The formation of unisexual flowers in maize requires the selective elimination and sexual maturation of floral organs in an initially bisexual floral meristem. Elimination of pistil primordia occurs in the primary and secondary florets of the tassel spikelets, and in the secondary florets of ear spikelets. Ill-fated pistil cells undergo a cell death process associated with nuclear degeneration in a specific spatial-temporal pattern that begins in the subepidermis, eventually aborting the entire organ. The sex determination genes tasselseed1 and tasselseed2 are required for death of pistil cells. tasselseed1 is required for the accumulation of TASSELSEED2 mRNA in pistil cells. All pistil primordia express TASSELSEED2 RNA but functional pistils found in ear spikelets are protected from cell death by the action of the silkless1 gene. silkless1 blocks tasselseed-induced cell death in the pistil primordia of primary ear florets. A model is proposed for the control of pistil fate by the action of the ts1-ts2-sk1 pathway.

2012 ◽  
Vol 4 (9) ◽  
pp. 964-979 ◽  
Author(s):  
Carla E. Cano ◽  
María José Sandí ◽  
Tewfik Hamidi ◽  
Ezequiel L. Calvo ◽  
Olivier Turrini ◽  
...  

2001 ◽  
Vol 1 (S3) ◽  
pp. 50-50
Author(s):  
M. Alonso ◽  
M. Miglaccio ◽  
I. Encio ◽  
A. Asumendi ◽  
V. Martinez-Merino ◽  
...  

Author(s):  
Carl D. Bortner ◽  
John A. Cidlowski

The movement of water across the cell membrane is a natural biological process that occurs during growth, cell division, and cell death. Many cells are known to regulate changes in their cell volume through inherent compensatory regulatory mechanisms. Cells can sense an increase or decrease in their cell volume, and compensate through mechanisms known as a regulatory volume increase (RVI) or decrease (RVD) response, respectively. The transport of sodium, potassium along with other ions and osmolytes allows the movement of water in and out of the cell. These compensatory volume regulatory mechanisms maintain a cell at near constant volume. A hallmark of the physiological cell death process known as apoptosis is the loss of cell volume or cell shrinkage. This loss of cell volume is in stark contrast to what occurs during the accidental cell death process known as necrosis. During necrosis, cells swell or gain water, eventually resulting in cell lysis. Thus, whether a cell gains or loses water after injury is a defining feature of the specific mode of cell death. Cell shrinkage or the loss of cell volume during apoptosis has been termed apoptotic volume decrease or AVD. Over the years, this distinguishing feature of apoptosis has been largely ignored and thought to be a passive occurrence or simply a consequence of the cell death process. However, studies on AVD have defined an underlying movement of ions that result in not only the loss of cell volume, but also the activation and execution of the apoptotic process. This review explores the role ions play in controlling not only the movement of water, but the regulation of apoptosis. We will focus on what is known about specific ion channels and transporters identified to be involved in AVD, and how the movement of ions and water change the intracellular environment leading to stages of cell shrinkage and associated apoptotic characteristics. Finally, we will discuss these concepts as they apply to different cell types such as neurons, cardiomyocytes, and corneal epithelial cells.


Blood ◽  
2007 ◽  
Vol 110 (12) ◽  
pp. 3978-3984 ◽  
Author(s):  
Silke F. Fischer ◽  
Philippe Bouillet ◽  
Kristy O'Donnell ◽  
Amanda Light ◽  
David M. Tarlinton ◽  
...  

Abstract T cell–dependent B-cell immune responses induce germinal centers that are sites for expansion, diversification, and selection of antigen-specific B cells. During the immune response, antigen-specific B cells are removed in a process that favors the retention of cells with improved affinity for antigen, a cell death process inhibited by excess Bcl-2. In this study, we examined the role of the BH3-only protein Bim, an initiator of apoptosis in the Bcl-2–regulated pathway, in the programmed cell death accompanying an immune response. After immunization, Bim-deficient mice showed persistence of both memory B cells lacking affinity-enhancing mutations in their immunoglobulin genes and antibody-forming cells secreting low-affinity antibodies. This was accompanied by enhanced survival of both cell types in culture. We have identified for the first time the physiologic mechanisms for killing low-affinity antibody-expressing B cells in an immune response and have shown this to be dependent on the BH3-only protein Bim.


2001 ◽  
Vol 1 ◽  
pp. 50-50
Author(s):  
M. Alonso ◽  
M. Miglaccio ◽  
I. Encío ◽  
A. Asumendi ◽  
V. Martinez-Merino ◽  
...  

2021 ◽  
Vol 13 (5) ◽  
Author(s):  
Carla E Cano ◽  
María José Sandí ◽  
Tewfik Hamidi ◽  
Ezequiel L Calvo ◽  
Olivier Turrini ◽  
...  

10.1038/8706 ◽  
1999 ◽  
Vol 22 (1) ◽  
pp. 115-115 ◽  
Author(s):  
Fredérique Quignon

1994 ◽  
Vol 11 (3) ◽  
pp. 447-454 ◽  
Author(s):  
Benjamin E. Reese ◽  
Janal L. Urich

AbstractNaturally occurring cell death has been hypothesized to sculpt various features of the organization of the mature visual pathways, including the recent proposal that the selective elimination of ganglion cells in the temporal retina shapes the formation of decussation patterns. Through a class-specific interocular competition, ganglion cells in the two temporal hemiretinae are selectively lost to produce the decussation patterns characteristic of each individual cell class (Leventhal et al., 1988). The present study has tested this hypothesis by asking whether the removal of one retina in newborn ferrets, which should disrupt binocular interactions at the level of the terminals, alters the decussation pattern of the alpha cells, a cell class that is entirely decussating in the normal adult ferret. Enucleation on the day of birth was found to increase the uncrossed projection by ≈50%, but not a single uncrossed alpha cell was found in the temporal retina. Either alpha cells never project ipsilaterally during development, or if they do, they cannot be rescued by early enucleation. While naturally occurring cell death plays many roles during development, creating the decussation pattern of the ferreth's alpha cell class via a binocular competition at the level of the targets is unlikely to be one of them.


2018 ◽  
Vol 9 ◽  
Author(s):  
Elodie Tenconi ◽  
Matthew F. Traxler ◽  
Charline Hoebreck ◽  
Gilles P. van Wezel ◽  
Sébastien Rigali

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