Bet-hedging and variability in plant development: seed germination and beyond.

When future conditions are unpredictable, bet-hedging strategies can be advantageous. This can involve isogenic individuals producing different phenotypes, under the same environmental conditions. Ecological studies provide evidence that variability in seed germination time has been selected for as a bet-hedging strategy. We demonstrate how variability in germination time found in Arabidopsis could function as a bet-hedging strategy in the face of unpredictable lethal stresses. Despite a body of knowledge on how the degree of seed dormancy versus germination is controlled, relatively little is known about how differences between isogenic seeds in a batch are generated. We review proposed mechanisms for generating variability in germination time and the current limitations and new possibilities for testing the model predictions. We then look beyond germination to the role of variability in seedling and adult plant growth and review new technologies for quantification of noisy gene expression dynamics. We discuss evidence for phenotypic variability in plant traits beyond germination being under genetic control and propose that variability in stress response gene expression could function as a bet-hedging strategy. We discuss open questions about how noisy gene expression could lead to between-plant heterogeneity in gene expression and phenotypes. This article is part of a discussion meeting issue 'Causes and consequences of stochastic processes in development and disease'.

Deubiquitinases in Neurodegeneration.

Ubiquitination refers to the conjugation of the ubiquitin protein (a small protein highly conserved among eukaryotes) to itself or to other proteins through differential use of ubiquitin's seven internal linkage sites or the amino-terminal amino group. By creating different chain lengths, an enormous proteomic diversity may be formed. This creates a signaling system that is central to controlling almost every conceivable protein function, from proteostasis to regulating enzyme function and everything in between. Protein ubiquitination is reversed through the activity of deubiquitinases (DUBs), enzymes that function to deconjugate ubiquitin from itself and protein substrates. DUBs are regulated through several mechanisms, from controlled subcellular localization within cells to developmental and tissue specific expression. Misregulation of DUBs has been implicated in several diseases including cancer and neurodegeneration. Here we present a brief overview of the role of DUBs in neurodegeneration, and as potential therapeutic targets.

The Molecular Basis of Spinocerebellar Ataxia Type 7.

Spinocerebellar ataxia (SCA) type 7 (SCA7) is caused by a CAG trinucleotide repeat expansion in the ataxin 7 (ATXN7) gene, which results in polyglutamine expansion at the amino terminus of the ATXN7 protein. Although ATXN7 is expressed widely, the best characterized symptoms of SCA7 are remarkably tissue specific, including blindness and degeneration of the brain and spinal cord. While it is well established that ATXN7 functions as a subunit of the Spt Ada Gcn5 acetyltransferase (SAGA) chromatin modifying complex, the mechanisms underlying SCA7 remain elusive. Here, we review the symptoms of SCA7 and examine functions of ATXN7 that may provide further insights into its pathogenesis. We also examine phenotypes associated with polyglutamine expanded ATXN7 that are not considered symptoms of SCA7.

Function and regulation of the Spt-Ada-Gcn5-Acetyltransferase (SAGA) deubiquitinase module.

The Spt-Ada-Gcn5 Acetyltransferase (SAGA) chromatin modifying complex is a critical regulator of gene expression and is highly conserved across species. Subunits of SAGA arrange into discrete modules with lysine aceyltransferase and deubiquitinase activities housed separately. Mutation of the SAGA deubiquitinase module can lead to substantial biological misfunction and diseases such as cancer, neurodegeneration, and blindness. Here, we review the structure and functions of the SAGA deubiquitinase module and regulatory mechanisms acting to control these.

Is the plant nucleus a mechanical rheostat?

Beyond its biochemical nature, the nucleus is also a physical object. There is accumulating evidence that its mechanics plays a key role in gene expression, cytoskeleton organization, and more generally in cell and developmental biology. Building on data mainly obtained from the animal literature, we show how nuclear mechanics may orchestrate development and gene expression. In other words, the nucleus may play the additional role of a mechanical rheostat. Although data from plant systems are still scarce, we pinpoint recent advances and highlight some differences with animal systems. Building on this survey, we propose a list of prospects for future research in plant nuclear mechanotransduction and development.

Mechanical Shielding in Plant Nuclei.

In animal single cells in culture, nuclear geometry and stiffness can be affected by mechanical cues, with important consequences for chromatin status and gene expression. This calls for additional investigation into the corresponding physiological relevance in a multicellular context and in different mechanical environments. Using the Arabidopsis root as a model system, and combining morphometry and micro-rheometry, we found that hyperosmotic stress decreases nuclear circularity and size and increases nuclear stiffness in meristematic cells. These changes were accompanied by enhanced expression of touch response genes. The nuclear response to hyperosmotic stress was rescued upon return to iso-osmotic conditions and could even lead to opposite trends upon hypo-osmotic stress. Interestingly, nuclei in a mutant impaired in the functions of the gamma-tubulin complex protein 3 (GCP3) interacting protein (GIP)/MZT1 proteins at the nuclear envelope were almost insensitive to such osmotic changes. The gip1gip2 mutant exhibited constitutive hyperosmotic stress response with stiffer and deformed nuclei, as well as touch response gene induction. The mutant was also resistant to lethal hyperosmotic conditions. Altogether, we unravel a stereotypical geometric, mechanical, and genetic nuclear response to hyperosmotic stress in plants. Our data also suggest that chromatin acts as a gel that stiffens in hyperosmotic conditions and that the nuclear-envelope-associated protein GIPs act as negative regulators of this response.