Seminiferous tubules in mammals have histological arrangements defined by the associations between somatic cells and germ cells. The processes of DNA synthesis in meiotic and mitotic cells have different features that are not easily distinguishable through morphological means. In order to characterize the pre-meiotic S phase, 5-bromo-2’-deoxyuridine (BrdU) was injected intraperitoneally into Wistar rats, which were sacrificed 30 min, 2 hr, and 24 hr after injection. We found three different labeling patterns. One of these patterns was characterized by a distribution of the label in the form of speckles, most of which were associated with the nuclear envelope (labeling type I). We suggest that this pattern is due to mitotic DNA synthesis of type B spermatogonia. Labeling type II consisted of labeled foci scattered throughout the nuclear volume, which can be correlated with preleptotenic cells in pre-meiotic DNA synthesis. After 24 hr of incorporation, a third type of labeling, characterized by large speckles, was found to be related to cells in the “bouquet” stage; that is, cells in transition between the leptotene and zygotene phases. Our results indicate that BrdU incorporation induces different labeling patterns in the mitotic and pre-meiotic S phases and thus makes it possible to identify somatic and germinal cells.

The nucleolus, once considered a mere ‘ribosome factory’, is now recognized as a dynamic hub influencing nearly every aspect of cellular life, from genome organization to stress response and ageing. Despite being a hallmark of eukaryotic cells, recent discoveries reveal that even prokaryotes exhibit nucleolus-like structures, hinting at ancient origins for nucleolar functions. This review explores the evolutionary journey of the nucleolus, tracing its roots back to early life and examining its structural and functional diversity across domains. We highlight key nucleolar proteins that play vital roles not only in ribosome production but also in regulating cell cycle, DNA repair and cellular stress, linking nucleolar activity directly to health and disease. Dysfunctions in nucleolar processes are implicated in cancer, ribosomopathies and neurodegenerative disorders, positioning the nucleolus as a critical target for innovative therapeutic strategies. As advanced imaging and molecular techniques unlock deeper insights into both canonical and mysterious non-canonical roles, the nucleolus stands as a model for how cellular microenvironments can evolve to meet complex biological demands. By addressing open questions surrounding the evolution of the nucleolus, its organization and diverse functions, the ideas presented here aim to contribute to the ongoing discussion, challenging traditional paradigms and suggesting new avenues for uncovering the fundamental principles that drive cellular life.

Metabolism, the network of biochemical reactions that powers life, arose under conditions radically different from those on Earth today. Investigating its origins reveals how initially simple chemical processes gradually integrated nucleic acid and then protein catalysts, becoming progressively more complex and regulated until they evolved into the enzyme-rich systems observed in modern organisms. Here, we integrate multiple perspectives on the origin of metabolism, focusing primarily on an evolutionary trajectory from an RNA-based world, where ribozymes, metal ions, coenzymes, small peptides, and other small organic molecules worked in concert, to enzyme-driven metabolic networks. We also address the longstanding debates on whether these early metabolic pathways were largely autotrophic or heterotrophic, and consider so-called “pre-metabolisms” (non-enzymatic networks) as an alternative conceptual framework. We discuss key examples such as the Wood–Ljungdahl (W–L) pathway and the reverse tricarboxylic acid (TCA) cycle, both posited to function under early Earth conditions. Finally, we examine how the environment (e.g., minerals, clays, hydrothermal vents) shaped early metabolism, describe unresolved questions about the Last Common Ancestor’s catalytic repertoire and propose future directions that link geochemical insights with molecular biology and synthetic approaches.

The catalytic, regulatory and structural properties of RNA, combined with their extraordinary ubiquity in cellular processes, are consistent with the proposal that this molecule played a much more conspicuous role in heredity and metabolism during the early stages of biological evolution. This review explores the pivotal role of RNA in the earliest life forms and its relevance in modern biological systems. It examines current models that study the early evolution of life, providing insights into the primordial RNA world and its legacy in contemporary biology.

Background Information: Autophagy is a conserved process that functions as a cytoprotective mechanism; it may function as a cell death process called programmed cell death type II. There is considerable evidence for the presence of autophagic cell death during oocyte elimination in prepubertal rats. However, the mechanisms involved in this process have not been deciphered.Results: Our observations revealed autophagic cell death in oocytes with increased labeling of the autophagic proteins Beclin 1, light chain 3 A (LC3 A), and lysosomal‐associated membrane protein 1 (Lamp1). Furthermore, mTOR and phosphorylated (p)‐mTOR (S2448) proteins were significantly decreased in oocytes with increased levels of autophagic proteins, indicating autophagic activation. Moreover, phosphorylated protein kinase B (p‐AKT) was not expressed by oocytes, but mitogen‐activated protein kinase/extracellular signalregulated kinase (MAPK/ERK) signaling was observed. Additionally, selective and elevated mitochondrial degradation was identified in altered oocytes.Conclusions: All these results suggest that mTOR downregulation, which promotes autophagy, could be mediated by low energy levels and sustained starvation involving the phosphoinositide 3‐kinase (PI3K)/AKT/mTOR and MAPK/ERK pathways.Significance: In this work, we analyzed the manner in which autophagy is carried out in oocytes undergoing autophagic cell death by studying the behavior of proteins involved in different steps of the autophagic pathway.