Efecto del volumen radicular sobre el crecimiento de Acacia dealbata Link. en vivero y en terreno en el secano de la Región del Biobío, Chile

Entre las especies arbóreas cultivadas en Chile, Acacia dealbata Link. se destaca por su rápido crecimiento y supervivencia en climas con marcado déficit hídrico y suelos altamente degradados. Aun cuando proporciona múltiples productos y servicios, la mayor parte de la investigación se ha centrado caracterizar su capacidad invasora, y poco se conoce respecto a su crecimiento durante los primeros años en terreno, escaseando antecedentes respecto efecto de la modificación de las prácticas silvícolas durante la producción y establecimiento de plantas. Por ello, este estudio analiza el efecto de la modificación del volumen radicular sobre el crecimiento durante la viverización, y la supervivencia y crecimiento culminadas la primera y segunda temporada en terreno. Finalizada la viverización resultó significativo el efecto del volumen radicular sobre el DAC y la altura total (P<0,05), los mayores valores se obtuvieron en plantas producidas con volumen de 100 cm³. Los volúmenes más altos presentaron los mayores índices de esbeltez y de Dickson (P<0.05), mientras que los mejores índices tallo/raíz se observaron con los volúmenes de 56 y 24 cm³ (P<0,05). Culminadas la primera y segunda temporada de crecimiento el efecto del volumen sobre la supervivencia resultó no significativo. Luego de la segunda temporada, se destacó el mayor incremento corriente anual en DAC del tratamiento de 24 cm³ (5,53 ± 1,63 mm). Luego de ambas temporadas se destacó una tendencia a la igualación en altura entre los tratamientos de 100, 80 y 24 cm³, el mayor crecimiento absoluto y relativo se observó en el tratamiento de 24 cm³

Non-canonical function of IRE1α determines mitochondria-associated endoplasmic reticulum composition to control calcium transfer and bioenergetics

Mitochondria-associated membranes (MAMs) are central microdomains that fine-tune bioenergetics by the local transfer of calcium from the endoplasmic reticulum to the mitochondrial matrix. Here, we report an unexpected function of the endoplasmic reticulum stress transducer IRE1α as a structural determinant of MAMs that controls mitochondrial calcium uptake. IRE1α deficiency resulted in marked alterations in mitochondrial physiology and energy metabolism under resting conditions. IRE1α determined the distribution of inositol-1,4,5-trisphosphate receptors at MAMs by operating as a scaffold. Using mutagenesis analysis, we separated the housekeeping activity of IRE1α at MAMs from its canonical role in the unfolded protein response. These observations were validated in vivo in the liver of IRE1α conditional knockout mice, revealing broad implications for cellular metabolism. Our results support an alternative function of IRE1α in orchestrating the communication between the endoplasmic reticulum and mitochondria to sustain bioenergetics

Publisher Correction: Non-canonical function of IRE1α determines mitochondria-associated endoplasmic reticulum composition to control calcium transfer and bioenergetics (Nature Cell Biology, (2019), 21, 6, (755-767), 10.1038/s41556-019-0329-y)

An amendment to this paper has been published and can be accessed via a link at the top of the paper

HIV Pretreatment Drug Resistance Trends in Mexico City, 2017&ndash;2020

In response to increasing pretreatment drug resistance (PDR), Mexico changed its national antiretroviral treatment (ART) policy, recommending and procuring second-generation integrase strand-transfer inhibitor (INSTI)-based regimens as preferred first-line options since 2019. We present a four-year observational study describing PDR trends across 2017&ndash;2020 at the largest HIV diagnosis and primary care center in Mexico City. A total of 6688 baseline protease-reverse transcriptase and 6709 integrase sequences were included. PDR to any drug class was 14.4% (95% CI, 13.6&ndash;15.3%). A significant increasing trend for efavirenz/nevirapine PDR was observed (10.3 to 13.6%, p = 0.02). No increase in PDR to second-generation INSTI was observed, remaining under 0.3% across the study period. PDR was strongly associated with prior exposure to ART (aOR: 2.9, 95% CI: 1.9&ndash;4.6, p &lt; 0.0001). MSM had higher odds of PDR to efavirenz/nevirapine (aOR: 2.0, 95% CI: 1.0&ndash;3.7, p = 0.04), reflecting ongoing transmission of mutations such as K103NS and E138A. ART restarters showed higher representation of cisgender women and injectable drug users, higher age, and lower education level. PDR to dolutegravir/bictegravir remained low in Mexico City, although further surveillance is warranted given the short time of ART optimization. Our study identifies demographic characteristics of groups with higher risk of PDR and lost to follow-up, which may be useful to design differentiated interventions locally

Genotoxic stress triggers the activation of IRE1α-dependent RNA decay to modulate the DNA damage response

International audienceThe molecular connections between homeostatic systems that maintain both genome integrity and proteostasis are poorly understood. Here we identify the selective activation of the unfolded protein response transducer IRE1α under genotoxic stress to modulate repair programs and sustain cell survival. DNA damage engages IRE1α signaling in the absence of an endoplasmic reticulum (ER) stress signature, leading to the exclusive activation of regulated IRE1α-dependent decay (RIDD) without activating its canonical output mediated by the transcription factor XBP1. IRE1α endoribonuclease activity controls the stability of mRNAs involved in the DNA damage response, impacting DNA repair, cell cycle arrest and apoptosis. The activation of the c-Abl kinase by DNA damage triggers the oligomerization of IRE1α to catalyze RIDD. The protective role of IRE1α under genotoxic stress is conserved in fly and mouse. Altogether, our results uncover an important intersection between the molecular pathways that sustain genome stability and proteostasis

Genotoxic stress triggers the activation of IRE1α-dependent RNA decay to modulate the DNA damage response.

The molecular connections between homeostatic systems that maintain both genome integrity and proteostasis are poorly understood. Here we identify the selective activation of the unfolded protein response transducer IRE1α under genotoxic stress to modulate repair programs and sustain cell survival. DNA damage engages IRE1α signaling in the absence of an endoplasmic reticulum (ER) stress signature, leading to the exclusive activation of regulated IRE1α-dependent decay (RIDD) without activating its canonical output mediated by the transcription factor XBP1. IRE1α endoribonuclease activity controls the stability of mRNAs involved in the DNA damage response, impacting DNA repair, cell cycle arrest and apoptosis. The activation of the c-Abl kinase by DNA damage triggers the oligomerization of IRE1α to catalyze RIDD. The protective role of IRE1α under genotoxic stress is conserved in fly and mouse. Altogether, our results uncover an important intersection between the molecular pathways that sustain genome stability and proteostasis