Cytokinins are involved in the regulation of many plant growth and development processes, and function in response to abiotic stress. Cytokinin signaling is similar to the prokaryotic two-component signaling systems and includes the transcriptional upregulation of type-A response regulators (RRs), which in turn act to inhibit cytokinin signal response via negative feedback. Cytokinin signaling consists of several gene families and only a handful full of genes is studied. In this study, we demonstrated the function of two highly identical type-A RR genes from rice, OsRR9 and OsRR10, which are induced by cytokinin and only OsRR10 repressed by salinity stress in rice. Loss-of-function mutations give rise to mutant genes, osrr9/osrr10, which have higher salinity tolerance than wild type rice seedlings. The transcriptomic analysis uncovered several ion transporter genes, which were upregulated in response to salt stress in the osrr9/osrr10 mutants relative to the wild type seedlings. These include high-affinity potassium transporters, such as OsHKT1;1, OsHKT1;3 and OsHKT2;1, which play an important role in sodium and potassium homeostasis. In addition, disruption of the genes OsRR9 and OsRR10 also affects the expression of multiple genes related to photosynthesis, transcription and phytohormone signaling. Taken together, these results suggest that the genes OsRR9 and OsRR10 function as negative regulators in response to salinity in rice.
CELLULAR FEEDBACK NETWORKS AND THEIR RESILIENCE AGAINST MUTATIONS
Many tissues undergo a steady turnover, where cell divisions are on average balanced with cell deaths. Cell fate decisions such as stem cell (SC) differentiations, proliferations, or differentiated cell (DC) deaths, may be controlled by cell populations through cell-to-cell signaling. Here, we examine a class of mathematical models of turnover in SC lineages to understand engineering design principles of control (feedback) loops, that may operate in such systems. By using ordinary differential equations that describe the co-dynamics of SCs and DCs, we study the effect of different types of mutations that interfere with feedback present within cellular networks. For instance, we find that mutants that do not participate in feedback are less dangerous in the sense that they will not rise from low numbers, whereas mutants that do not respond to feedback signals could rise and replace the wild-type population. Additionally, we asked if different feedback networks can have different degrees of resilience against such mutations. We found that all minimal networks, that is networks consisting of exactly one feedback loop that is sufficient for homeostatic stability of the wild-type population, are equally vulnerable. Mutants with a weakened/eliminated feedback parameter might expand from lower numbers and either enter unlimited growth or reach an equilibrium with an increased number of SCs and DCs. Therefore, from an evolutionary viewpoint, it appears advantageous to combine feedback loops, creating redundant feedback networks. Interestingly, from an engineering prospective, not all such redundant systems are equally resilient. For some of them, any mutation that weakens/eliminates one of the loops will lead to a population growth of SCs. For others, the population of SCs can actually shrink as a result of “cutting” one of the loops, thus slowing down further unwanted transformations.
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- Award ID(s):
- 1763272
- NSF-PAR ID:
- 10222821
- Date Published:
- Journal Name:
- Journal of Biological Systems
- ISSN:
- 0218-3390
- Page Range / eLocation ID:
- 1 to 50
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Journal Article:
- https://doi.org/10.1142/S0218339021400039
