A receptor-like protein mediates the response to pectin modification by activating brassinosteroid signaling.
نویسندگان
چکیده
The brassinosteroid (BR) signaling module is a central regulator of plant morphogenesis, as indicated by the large number of BR-responsive cell wall-related genes and the severe growth defects of BR mutants. Despite a detailed knowledge of the signaling components, the logic of this auto-/paracrine signaling module in growth control remains poorly understood. Recently, extensive cross-talk with other signaling pathways has been shown, suggesting that the outputs of BR signaling, such as gene-expression changes, are subject to complex control mechanisms. We previously provided evidence for a role of BR signaling in a feedback loop controlling the integrity of the cell wall. Here, we identify the first dedicated component of this feedback loop: a receptor-like protein (RLP44), which is essential for the compensatory triggering of BR signaling upon inhibition of pectin de-methylesterification in the cell wall. RLP44 is required for normal growth and stress responses and connects with the BR signaling pathway, presumably through a direct interaction with the regulatory receptor-like kinase BAK1. These findings corroborate a role for BR in controlling the sensitivity of a feedback signaling module involved in maintaining the physico-chemical homeostasis of the cell wall during cell expansion.
منابع مشابه
Plant Cell Wall Homeostasis Is Mediated by Brassinosteroid Feedback Signaling
Brassinosteroid (BR) signaling is required for normal plant growth as shown by the dwarf phenotype of loss-of-function BR biosynthetic or perception mutants. Despite a detailed understanding of the BR signaling network, it is not clear how exactly BRs control growth. For instance, genetic sector analysis shows that BRs, in contrast to most other growth regulators, act locally, presumably in an ...
متن کاملP 143: The Effect of Platelet Activating Factor on Inflammatory Response in Multiple Sclerosis
Multiple sclerosis is an autoimmune disease of the central nervous system which its main characteristic is an inflammation and demyelination and subsequent, neural degeneration. Many studies have shown that inflammation causing neuronal demyelination. MS is the most common cause of chronic neurological disability in during youth which the prognosis is that can be death. Platelet activating fact...
متن کاملThe Implication of Androgens in the Presence of Protein Kinase C to Repair Alzheimer’s Disease-Induced Cognitive Dysfunction
Aging, as a major risk factor of memory deficiency, affects neural signaling pathways in hippocampus. In particular, age-dependent androgens deficiency causes cognitive impairments. Several enzymes like protein kinase C (PKC) are involved in memory deficiency. Indeed, PKC regulatory process mediates α-secretase activation to cleave APP in β-amyloid cascade and tau proteins phosphorylation mecha...
متن کاملEffect of Exogenous Brassinosteroid Application on Grain Yield, some Physiological Traits and Expression of Genes Related to This Hormone Signaling Pathway in Wheat under Drought Stress
To investigate the effect of exogenous brassinosteroid application on grain yield, catalase, chlorophyll content, membrane mtability index and gene expression of some genes involving in brassinosteroid signaling pathway (BES1 and BRI1) under drought stress, a split-split plot on randomized complete block design with three replications was conducted at the experimental field of Seed and Plant Im...
متن کاملO-13: Na+/K+-ATPase Alpha1 Isoform Mediates Ouabain-Induced Expression of Cyclin D1 and Proliferation of Rat Sertoli Cells
Background: Novel roles for the interaction of cardiotonic steroids to Na+/K+-ATPase have been established in recent years. The aim of the present study was to investigate the intracellular signaling events downstream the action of ouabain on Na+/K+-ATPase in Sertoli cell obtained from immature rats. Treatment of Sertoli cells with ouabain (1 μM) induced a rapid and transient increase in the ex...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Proceedings of the National Academy of Sciences of the United States of America
دوره 111 42 شماره
صفحات -
تاریخ انتشار 2014