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Das, S. S.

Publications and source records attributed to Das, S. S..

2 recordsLinked to original sources

MicroRNA775 and target Galactosyltransferase (GALT9) module regulates recovery from submergence induced senescence by modulating SAGs in Arabidopsis thaliana

Submergence induced hypoxic condition is one of the abiotic stresses which negatively affects the plant growth and development, and causes early onset of senescence. Hypoxic conditions ateres the expression of a number of non-coding microRNAs (miRNAs), besides protein-coding genes. However, the molecular function of stress-induced miRNA in submergence induced physiological or developmental changes and recovery remains to be understood. The expression of miR775 is highly induced under hypoxic stress conditions. Here, we show that miR775 is a potential post-transcriptional regulator number of targets, including Galactosyltransferase (GALT9). The expression of miR775 and target GALT9 was significantly induced and reduced respectively at 24 hours of submergence. The overexpression of miR775 (miR775-Oe) confers enhanced recovery from submergence stress and reduced accumulation of ROS, in contrast to wild type and endogenous target mimic of miR775 (MIM775) Arabidopsis plants. We observed a similar recovery phenotype in case of target galt9 mutant plants, indicating the role of miR775-GALT9 module in recovery from submergence. Further, we showed that the expression of SENESCENCE ASSOCIATED GENES (SAGs), such as SAG12, SAG29, and ORE1. was increased in MIM775 and reduced in miR775-Oe and galt9 plants. Thus, our results suggest that miR775-GALT9 module plays a crucial role in the recovery from submergence by modulating the expression of SAGs through differential accumulation of ROS.

plant biology↗

Antagonistic activities of Fmn2 and ADF regulate axonal F-actin patch dynamics and the initiation of collateral branching

Interstitial collateral branching of axons is a critical component in the development of functional neural circuits. Axon collateral branches are established through a series of cellular processes initiated by the development of a specialized, focal F-actin network in axons. The formation, maintenance and remodelling of this F-actin patch is critical for the initiation of axonal protrusions that are subsequently consolidated to form a collateral branch. However, the mechanisms regulating F-actin patch dynamics are poorly understood. Fmn2 is a formin family member implicated in multiple neurodevelopmental disorders. We find that Fmn2 regulates the initiation of axon collateral protrusions. Fmn2 localises to the protrusion-initiating axonal F-actin patches and regulates the lifetime and size of these F-actin networks. The F-actin nucleation activity of Fmn2 is necessary for F-actin patch stability but not for initiating patch formation. We show that Fmn2 insulates the F-actin patches from disassembly by the actin-depolymerizing factor, ADF, and promotes long-lived, larger patches that are competent to initiate axonal protrusions. The regulation of axonal branching can contribute to the neurodevelopmental pathologies associated with Fmn2 and the dynamic antagonism between Fmn2 and ADF may represent a general mechanism of formin-dependent protection of Arp2/3-initiated F-actin networks from disassembly.

neuroscience↗