In plants, aerial organs are initiated at stereotyped intervals, both spatially (every 137° in a pattern called phyllotaxis) and temporally (at prescribed time intervals called plastochrons). To investigate the molecular basis of such regularity, mutants with altered architecture have been isolated. However, most of them only exhibit plastochron defects and/or produce a new, albeit equally reproducible, phyllotactic pattern. This leaves open the question of a molecular control of phyllotaxis regularity. Here, we show that phyllotaxis regularity depends on the function of VIP proteins, components of the RNA polymerase II-associated factor 1 complex (Paf1c). Divergence angles between successive organs along the stem exhibited increased variance in vip3-1 and vip3-2 compared with the wild type, in two different growth conditions. Similar results were obtained with the weak vip3-6 allele and in vip6, a mutant for another Paf1c subunit. Mathematical analysis confirmed that these defects could not be explained solely by plastochron defects. Instead, increased variance in phyllotaxis in vip3 was observed at the meristem and related to defects in spatial patterns of auxin activity. Thus, the regularity of spatial, auxin-dependent, patterning at the meristem requires Paf1c.

To date, Ag-based nanomaterials have demonstrated a high potential to overcome antibiotic resistance issues. However, bare Ag nanomaterials are prone to agglomeration in the biological environment, which results in a loss of antibacterial activity over time. Furthermore, it is still challenging to collect small-sized Ag nanomaterials right after the synthesis process. In this study, spherical-shaped Ag nanoparticles (NPs) (~6–10 nm) were attached on the surface of cetyltrimethylammonium bromide (CTAB)-loaded mesoporous silica nanoparticles (MSNs) (~100–110 nm). Antibacterial activity tests suggested that the obtained nanocomposite can be used as a highly efficient antibacterial agent against both Gram-negative and Gram-positive bacterial strains. The minimum inhibitory concentration (MIC) recalculated to pure Ag weight in nanocomposite was found to be ~1.84 µg/mL (for Escherichia coli) and ~0.92 µg/mL (for Staphylococcus aureus)—significantly smaller compared to values reported to date. The improved antibacterial activity of the prepared nanocomposite can be attributed to the even distribution of non-aggregated Ag NPs per volume unit and the presence of CTAB in the nanocomposite pores.

The etiology of childhood cancers has been studied for more than 40 years. However, most if not all cancers occurring in children are attributed to unknown causes. This review is focused on the role of infections in cancer development and progression in children. The main infectious agents include human herpesviruses, polyoma viruses, and human papilloma viruses. It is known that infections can lead to carcinogenesis through various mechanisms, and most likely act in addition to genetic and environmental factors. Given the importance of the infectious etiology of childhood cancers, clinical implications and possible prevention strategies are discussed.

The regulation of cancerous tumor development is converged upon by multiple pathways and factors. Besides environmental factors, gastrointestinal (GI) tract cancer can be caused by chronic inflammation, which is generally induced by bacteria, viruses, and parasites. The role of these inducers in cancer development, cell differentiation and transformation, cell cycle deregulation, and in the expression of tumor-associated genes cannot be ignored. Although Helicobacter pylori activates many oncogenic pathways, particularly those in gastric and colorectal cancers, the role of viruses in tumor development is also significant. Viruses possess significant oncogenic potential to interfere with normal cell cycle control and genome stability, stimulating the growth of deregulated cells. An increasing amount of recent data also implies the association of GI cancers with bacterial colonization and viruses. This review focuses on host-cell interactions that facilitate primary mechanisms of tumorigenesis and provides new insights into novel GI cancer treatments.