Invited Review: Somatotropin and Lactation BiologyCollier, Bauman, Baumgard
J Dairy Sci (2025)
Abstract: Purpose of this review is to update the human and animal safety findings on bovine somatotropin (bST) since 1993 as well as to discuss ST action and its impacts on sustainability. Bovine somatotropin (bST) is a naturally produced hormone which is a key regulator of growth and milk production. Beginning in the 1930s and continuing until today, investigations have examined bST's impact on animal related factors such as nutrition, bioenergetics, metabolism, health, and well-being, and consumer related issues such as product safety, milk quality, and manufacturing characteristics. Overall, bST homeorhetically orchestrates (both directly and indirectly) the coordination of key physiological processes involved in lactation. Bovine somatotropin's direct effects involve adaptations in a variety tissues, and altered metabolism of all nutrient classes - water, carbohydrates, lipids, protein, and minerals. Mechanistically, this includes modifying key enzymes, intracellular signal transduction systems, tissue response to homeostatic signals and diversity of receptor subtypes. Indirect effects are mediated by the insulin-like growth factor (IGF) system. Collectively, IGF governs cellular changes within the mammary gland resulting in increased rates of milk synthesis and enhanced maintenance of secretory cells. The responses to bST are modulated by environmental and management factors, especially an animal's nutritional plane. This modulation is a principal component in allowing bST to play a key role in regulating nutrient utilization across a range of physiological states. Recombinant bST (rbST) was developed in the early 1980s and commercial rbST use in the United States began in 1994. Utilizing rbST markedly increases milk yield and improves feed efficiency and farm income; thus, it was rapidly adopted by many dairy producers. Despite reducing the environmental footprint of milk production and having no impact on cow health in well-managed dairies, milk consumption or human safety concerns, many within the processing, grocery and retailer industries began labeling and promoting "rbST-free" dairy products as a marketing strategy. The FDA was concerned this represented an implied health issue, so they required products labeled as "rbST-free" to also include the statement that "no significant difference has been shown between milk derived from rbST treated and non-rbST treated cows." Many Cooperatives had an aggressive strategy to market "rbST-free" milk to compete with "organic" milk and suggested producers would receive higher milk prices if they voluntarily stopped using rbST. The net effect was American farmers ceased using the technology. However, rbST continues to safely increase farmer revenue and to minimize the carbon footprint of dairy production in many parts of Asia, Africa, and South America. Overall, bST is a homeorhetic control which orchestrates metabolic processes affecting nutrient partitioning and animal productivity, and it is naturally higher in genetically superior animals. The intrinsic biology of endogenous bST can be harnessed with the use of exogenous rbST to safely and sustainably improve animal performance.© 2025, The Authors. Published by Elsevier Inc. on behalf of the American Dairy Science Association®. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Microscopy-based methods for characterizing autophagy and understanding its dynamics in resin secretionde Carvalho, Scudeler, Machado
Micron (2025) 192-193, 103818
Abstract: Resin-secretory canals are a common feature of Anacardiaceae plants, and their resins have widespread applications in both industry and medicine. Cytological evidence strongly supports the occurrence of autophagy during the development of resin-secreting glands in several species of this family, including Anacardium humile. However, systematic investigations focusing on this process in these glands remain limited. This study aimed to enhance our understanding of autophagy in A. humile resin glands by elucidating its occurrence, timing, and specific mechanisms during the secretory cycle. Standard transmission electron microscopy techniques were used in conjunction with the cytochemical assays. Immunogold labeling and confocal immunofluorescence studies were conducted to identify autophagosomes and other autophagy-related structures. Two distinct types of autophagy have been identified, each associated with a specific phase of the secretory cycle. Macroautophagy predominates at the peak of secretion, whereas microautophagy occurs during the final stages of the cycle. As an integral component of the secretory process, autophagosomes degrade cytoplasmic components and organelles before fusing with the lysosomal vacuoles. In contrast to previous studies reporting extensive cellular degradation at the end of the resin-secretory cycle, often interpreted as a form of programmed cell death, no evidence of mega-autophagy was observed in this study. These findings suggest that the precise regulation of autophagy timing and intensity is crucial for maintaining the functional integrity of resin-secreting cells. Furthermore, the potential interplay between autophagic activity and terpene biosynthesis requires further investigation in the context of resin-secretory canal physiology.Copyright © 2025. Published by Elsevier Ltd.
Programmed cell senescence is required for sensory organ development in DrosophilaZang, Yoshimoto, Igaki
iScience (2025) 28 (3), 112048
Abstract: Cellular senescence is an irreversible cell-cycle arrest often associated with cancer and aging, yet its physiological role remains elusive. Here, we show developmentally programmed cellular senescence occurs in Drosophila imaginal epithelium. In developing wing discs, two clusters of cells exhibit hallmarks of cellular senescence such as elevated senescence-associated β-galactosidase activity, cell-cycle arrest, heterochromatinization, upregulation of a cyclin-dependent kinase (CDK) inhibitor Dacapo, cellular hypertrophy, Ras signaling activation, and upregulation of an inflammatory cytokine unpaired3, a possible component of the senescence-associated secretory phenotype. Blocking programmed cell senescence by inhibiting Ras signaling or its downstream transcription factor Pointed (Pnt) results in loss of sensory organ campaniform sensilla. Ras-Pnt signaling causes programmed cell senescence through a transcription factor Zfh2, thereby contributing to campaniform sensilla formation via the achaete-scute complex. Our observations uncover the evolutionary conservation of programmed cell senescence in invertebrates, which is required for the induction of the proper number of sensory organs.© 2025 The Author(s).
Clinical, biochemical and cell biological characterization of KIDAR syndrome associated with a novel AP1B1 variantKaniganti, Gean-Akriv, Keidar
et alMol Genet Metab (2025) 144 (4), 109056
Abstract: Adaptor protein (AP) complexes play key roles in escorting transmembrane proteins to various intracellular destinations, including the trans-Golgi compartment, secretory vesicles, and the plasma membrane. The AP-1 complex is heterotetrametric, comprised of four individual subunits: β1, γ1, σ1, and μ1, and encoded by separate genes that interact selectively with distinct cargo proteins. When AP-1 complex assembly is impaired due to loss-of-function variants in any of its component genes, clinical consequences related to altered transmembrane protein trafficking may result. Biallelic pathogenic variants in the β1 subunit (AP1B1) are associated with a unique clinical phenotype including keratitis, ichthyosis, and deafness with autosomal recessive inheritance, the KIDAR syndrome. This disorder is further characterized by enteropathy, failure to thrive, neurodevelopmental delays, endocrinopathies, and abnormalities in copper (Cu) metabolism, the latter reflecting impact on intracellular trafficking of two transmembrane Cu-transporting ATPases, ATP7A and ATP7B. Ten individuals with KIDAR syndrome have been reported to date. Here we describe the clinical, biochemical, and cell biological effects associated with a novel homozygous AP1B1 variant, (NM_001127.4: c.667delC, p.Leu223Trp*fsTer38) in a previously unreported individual. Our findings expand the phenotypic spectrum of this rare inherited illness, provide new data related to its cell biological effects, and offer insights relevant to potential treatment.Copyright © 2025 The Authors. Published by Elsevier Inc. All rights reserved.
膜杰作
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