Release From Post-transcriptional Gene Silencing by Cell Proliferation in Transgenic Tobacco Plants: Possible Mechanism for Noninheritance of the Silencing

Abstract

Transgenic tobacco plants that overproduce luciferase (Luc) frequently exhibit post-transcriptional gene silencing (PTGS) of luc. The silencing was observed over five generations and found not to be inherited but acquired by the next generation at a certain frequency. Luc imaging analysis of silenced plants revealed Luc activity only in proliferating tissues such as shoot meristem and developing flower. The luc gene expression has been recovered from silencing before development of germ cells, excluding a possible recovery from the PTGS at meiosis. A systemic silencing signal transferred from older tissue likely induces gene silencing of younger tissues in which cell proliferation has been completed. Only seeds maintained Luc activity, probably because of isolation from the silencing signal by a possible partition from the parent placenta. Calli newly induced from the leaf pieces of silenced plants recovered from the silencing and exhibited strong Luc activity similar to nonsilenced leaves, further indicating that the silencing cannot be maintained in proliferating cells. Thus release from PTGS in proliferating cells is a possible mechanism for noninheritance of silencing.

High temperature increases centromere-mediated genome elimination frequency and enhances haploid induction in Arabidopsis

“…Previously, it was shown that cenH3 levels in the cenH3 RNAi transformants were more strongly reduced in leaves than in root tips enriched in meristematic cells ( Lermontova et al., 2011 ). On the basis of previously published data, we hypothesized that this may be because of decreased activity of the cauliflower mosaic virus (CaMV) 35S promoter used ( Holtorf et al., 1995 ; Wang et al., 2015 ) and suppression of post-translational gene silencing in meristems and reproductive tissues, which may decrease the function of the RNAi machinery ( Mitsuhara et al., 2002 ). Using maize cenH3 RNAi lines complemented with the AcGREEN-tail swap-CENH3 , Kelliher et al.…”

High temperature increases centromere-mediated genome elimination frequency in Arabidopsis deficient in cenH3 or its assembly factor KNL2

“…Previously, it has been shown that the level of cenH3 in the cenH3 RNAi transformants was strongly reduced in leaves than in root tips enriched in meristematic cells (Lermontova et al ., 2011). Based on previously published data, we hypothesized that this may be due to a decreased activity of the CaMV 35S promoter (Holtorf et al ., 1995) and suppression of post-translational gene silencing in meristems, which may cause the ineffective function of the RNAi machinery in these tissues (Mitsuhara et al ., 2002). Using maize cenH3 RNAi lines complemented by the AcGREEN-tail swap-CENH3 , Kelliher et al .…”

Time-delayed model of immune response in plants

“…Laboratory studies have shown that the silenced state cannot be inherited directly, meaning that a parent cell will most likely be unable to produce daughter cells with the anti-viral components needed to deal with the viral infection. It is, therefore, believed that undifferentiated and proliferating cells, e.g meristematic tissue, need to mature or be released from cellular reproduction before they can acquire an antiviral state [25]. Hence, we introduce P (t) as the population of proliferating cells that are responsible for promoting new plant growth.…”

“…the system of equations ( 24) can be re-written as follows g 1 (τ 1 ) sin(wτ 1 ) − g 2 (τ 1 ) cos(wτ 1 ) = L 1 (τ 1 ), g 1 (τ 1 ) cos(wτ 1 ) + g 2 (τ 1 ) sin(wτ 1 ) = L 2 (τ 1 ). (25) Solving this system yields…”