Research & Internships

Antibiotics can enter the environment through sources such as wastewater, agricultural runoff, and human and animal waste. Especially when present at low concentrations that do not kill bacteria, they can affect bacterial growth and may contribute to the development and spread of antibiotic resistance. This review observes how prolonged exposure to sub-lethal or sub-MIC antibiotic concentrations affects bacterial growth and resistance development. Findings from previous studies were compared, focusing on growth curves, changes in lag phase, growth rate and final density, changes in MIC, resistance mutations, and horizontal gene transfer (HGT).

The studies showed that the response to sub-lethal antibiotic exposure was not always the same. Some antibiotics delayed bacterial growth, mainly by increasing the lag phase, while certain low concentrations also produced higher growth rates or final densities than the antibiotic-free control, suggesting a hormetic effect. Resistance was found to develop through the selection and accumulation of mutations in some studies, while others showed that sub-MIC exposure increased the transfer of existing resistance genes through HGT. Overall, the findings suggest that low antibiotic concentrations can put enough pressure on bacteria to favour resistance while still allowing them to survive and reproduce. This makes environmental antibiotic pollution a concern because resistance can develop or spread outside clinical settings. Future research should use longer exposure periods, more antibiotics and bacterial strains, and more realistic environmental conditions.

This paper explores how environmental stress can influence epigenetic regulation and change the way genes are expressed without altering the underlying DNA sequence. It focuses on mechanisms such as DNA methylation, histone modifications, chromatin structure, and non-coding RNAs, with particular attention to how these processes help plants respond to stresses such as drought, heat, cold, and salinity. The paper uses a literature-based approach, comparing findings from human studies, controlled plant and animal experiments, and epigenome-wide research rather than generating new experimental data. Different research methods, including bisulfite sequencing, ChIP-seq, and RNA sequencing, were also examined to understand how epigenetic changes are detected and analysed.

The literature shows that environmental exposure can produce measurable changes in the epigenome and influence stress-response genes, although these effects are often context- and tissue-specific. Comparisons between cold and heat stress also show that plants do not rely on one general epigenetic response. Some epigenetic changes may persist and contribute to stress memory, while studies of sperm RNA suggest that chemically modified RNAs can also carry environmental information between generations. However, distinguishing causation from correlation remains difficult, particularly because of reverse causation, tissue-access limitations, and other confounding factors. Overall, epigenetics appears to add an important regulatory layer to heredity and gene expression, but many questions about causal mechanisms, stability, and inheritance remain open.