Lateral roots (LRs) are a main component of the root system of rice (Oryza sativa) that increases root surface area, enabling efficient absorption water and nutrients. However, the molecular mechanism regulating LR formation in rice remains largely unknown. Here, we report that Histone Deacetylase 1 (OsHDAC1) positively regulates LR formation in rice. Rice OsHDAC1 RNAi plants produced fewer lateral roots than wild-type plants, whereas plants overexpressing OsHDAC1 exhibited increased lateral root proliferation by promoting LR primordia formation. Brassinosteroid treatment increased the LR number, as did mutation of GSK3/SHAGGY-like kinase 2 (OsGSK2), whereas overexpression of OsGSK2 decreased the LR number. Importantly, OsHDAC1 could directly interact with and deacetylate OsGSK2, inhibiting its activity. OsGSK2 deacetylation attenuated the interaction between OsGSK2 and BRASSINAZOLE RESISTANT 1 (OsBZR1), leading to accumulation of OsBZR1. Overexpression of OsBZR1 increased LR formation by regulating Auxin/IAA signaling genes. Taken together, the results indicate that OsHDAC1 regulates LR formation in rice by deactivating OsGSK2, thereby preventing degradation of OsBZR1, a positive regulator of LR primordia formation. Our findings suggest that OsHDAC1 is a breeding target in rice that can improve resource capture.

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The role of the nucleolus in plant response to heat stress remains largely obscure.Our current efforts focused on exploring the underlying mechanism by which nucleolar disorganization is regulated in heat stressed-maize lines. Here, two maize lines, a heat-sensitive line, ZD958, and a heat-tolerant line, ZDH, were submitted to heat

R-loops are both regulators in many cellular processes and threats to genome integrity. Understanding the mechanism underlying regulation of R-loops is very important. Inspired by the findings of RNase H1-mediated R-loop formation, we focus our interest on the regulation of RNase H1 recruitment and expression. Here we report that G9a not only boosts the recruitment of RNase H1 to reduce R-loop accumulation at the rDNA site, but also positively regulates RNase H1 expression, whereas CHCHD2 prevents RNase H1 from being recruited to rDNA site and acts as a repressive transcription factor to inhibit the expression of RNase H1 to increase R-loop formation. We also found that G9a methylated the promoter of the RNase H1 gene, which inhibited the binding of CHCHD2. By contrast, when G9a was knocked down, the recruitment of CHCHD2 and Sirt1 to the RNase H1 promoter increased, which co-inhibited the RNase H1 transcription. Furthermore, G9a could directly bind CHCHD2, possibly decreasing free CHCHD2. Sirt1 could interact with CHCHD2 and functioned as a repressor suppressing transcription of the RNase H1 gene. Knockdown of Sirt1 led to binding of more G9a to the RNase H1 promoter. Taken together, we demonstrate that G9a regulates the expression of RNase H1 to maintain the steady-state balance of R-loops by suppressing CHCHD2 and Sirt1 corepressors being recruited to the target gene promoter.