Samuels, A. | bioRxiv Science

bioRxiv2026

Light spectral quality alters glandular trichome architecture more strongly than cannabinoid accumulation in Cannabis sativa

The glandular trichomes in Cannabis sativa, found predominantly on female flowers, produce and store a variety of unique phytocannabinoids, increasingly studied for their use in medicinal applications. Maximizing yield and cannabinoid profiles requires the optimization of the environmental factors that regulate plant growth. Light plays a prominent role, both as an energy source but also as an important developmental signal. Thus, optimization of lighting strategies, particularly through customizable light-emitting diode (LED) fixtures, has become a major focus of controlled-environment cannabis research. Here, we focus on the effect of blue-enriched and far red-enriched light spectra on the morphological traits and biochemical profiles of two THCA-dominant varieties: Pineapple Cough and Rocky Fire #7. Spectral composition exerts modest and genotype-specific effects on the plant development, inflorescence biomass, and cannabinoid concentration but we demonstrate a positive correlation between total yield and plant height in both varieties, regardless of spectra. We also show that growth under far-red enriched light affects the visible pigmentation in both varieties with significantly lower chlorophyll levels and paler fan and sugar leaves. Finally, we demonstrate that far-red light consistently increased the trichome stalk length in both varieties, suggesting that spectral composition can alter trichome development and morphology. Our data offers insights into cannabis development and secondary chemical profiles in response to different light spectra, allowing growers to adjust light spectra to obtain desirable cannabis traits for industrial production.

Plant Biology↗

bioRxiv2022

Autophagy protects against high-dose Mycobacterium tuberculosis infection

Host autophagy had been associated with the control of Mycobacterium tuberculosis (Mtb) infection due to its ability to sequesters microorganisms through a process termed "xenophagy"1-4. Xenophagy purportedly limits Mtb replication within infected macrophages1-4. However, studies in mice using a standard low-dose infection model demonstrated that xenophagy in infected phagocytes is not required to control Mtb pathogenesis5,6. Instead, an autophagy-independent function of ATG5 in myeloid cells controls low-dose Mtb infection through limiting neutrophilic inflammation5. Hitherto, an in vivo role for autophagy during Mtb infection remained to be elucidated. We report herein that autophagy in myeloid cells mediates protection against high-dose Mtb infection, providing the first evidence for a role for autophagy in myeloid cells during Mtb infection in vivo. With the exception of ATG5, the autophagy proteins required to control high-dose Mtb infection are dispensable for host defense against a standard low-dose Mtb infection. Specifically, autophagy is required in CD11c+ cells, but is dispensable in neutrophils, to control a high-dose Mtb infection in the lung. The role for autophagy is not to directly degrade Mtb in macrophages through xenophagy, but mainly to limit myeloid-derived suppressor cell accumulation and to promote sustained protective T cell responses. Together, our data highlight a novel role for autophagy in controlling Mtb infection, distinct from that of Atg5 during low-dose Mtb infection, or any previously reported roles for autophagy. In addition, our finding that the result of a pathogen-plus-susceptibility gene interaction is dependent on pathogen burden has important implications on our understanding of how Mtb infection in humans can lead to a spectrum of outcomes, the variables that contribute to autophagy gene function during infection and inflammation, and the potential use of autophagy modulators in clinical medicine.

microbiology↗