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PubMed2025

Integrating hotspot dynamics and centers of diversity: a review of Indo-Australian Archipelago biogeographic evolution and conservation.

The Indo-Australian Archipelago (IAA) is the world's preeminent marine biodiversity hotspot, distinguished by its exceptional species richness in tropical shallow waters. This biodiversity has spurred extensive research into its evolutionary and biogeographic origins. Two prominent theoretical frameworks dominate explanations for the IAA's biodiversity: the "centers-of hypotheses" and the "hopping hotspot hypothesis". The "centers-of hypotheses" posits that specific regions serve as key sources of IAA biodiversity, either through the accumulation and overlap of species from external areas or via elevated rates of local speciation. In contrast, the "hopping hotspot hypothesis" asserts that biodiversity hotspots are dynamic, shifting across geological timescales in response to tectonic and environmental changes. This review synthesizes these contrasting perspectives into an integrated framework, the "Dynamic Centers Hypothesis," which proposes that as biodiversity hotspots migrate over time, the IAA's role in generating and sustaining biodiversity has evolved, with varying contributions from different sources dominating distinct historical phases. By synthesizing the evidence for both hypotheses and incorporating recent findings, including fossil and phylogeography data, we propose the "Dynamic Centers Hypothesis" as a comprehensive and unifying explanation for the IAA's biodiversity. The review further explores biogeographic delineation, aligning tropical marine realms with the IAA's evolutionary trajectory, from its Tethyan roots to its modern Indo-West Pacific dominance. Looking forward, advances in DNA barcoding and genomics are uncovering vast cryptic diversity, revolutionizing our comprehension of IAA phylogeographic history. These discoveries underscore the imperative for a multidimensional conservation framework, integrating phylogenetic, and functional diversity, to preserve this biodiversity hotspot amid escalating global change.

Biogeography↗

PubMed2026

Centromeres and telomeres as rheological probes of the human cell nucleus.

The human genome contains genetic information essential for life, controlling all cellular processes via the central dogma of biology. It is a canonical example of a living polymer, yet the physical principles underlying its dynamical self-organization in the cell nucleus remain unknown. In this work, we investigate the polymeric nature of the genome in live human cells, by studying motions of the centers and free ends of linear chromosome polymers-the centromeres and telomeres-and rheology of their nuclear environment. Our findings reveal that telomeres have 10-times larger displacements than centromeres, exceeding by far predictions of polymer theories. We find that this unexpectedly large difference arises due to centromere and telomere localization in unique nuclear environments, distinct in both their biological activity and material rheology. While the former resides in the genome's silenced parts, the latter localizes in its transcriptionally active parts. Our rheological analysis shows that centromeres are embedded in an elastic environment, whereas telomeres' surroundings are viscous, directly affecting timescales and length scales of their respective motions. Our results suggest a key role of nuclear heterogeneity in genome dynamics, which we corroborate by biochemical perturbations of nuclear structures such as heterochromatin and nuclear speckles. Finally, upon homogenizing the nuclear environment by a hypoosmotic shock, we observe equal centromeric and telomeric motions, confirming our hypothesis. Our observations show that the heterogeneity of nuclear environment directly impacts timescales and length scales of local genomic motions, which may affect the spatiotemporal gene regulation across the cell nucleus.

Humans↗

PubMed1979

Hormone receptor topology and dynamics: morphological analysis using ferritin-labeled epidermal growth factor.

Previous studies using a biologically active 1:1 conjugate of EGF and ferritin (F-EGF) have traced the binding and internalization of the hormone molecules. In the present report, we develop ultrastructural criteria for identification of the F-EGF.receptor complex, and, thereby, enable utilization of the F-EGF as an indirect marker to localize the receptor for this peptide hormone. The ferritin cores of bound F-EGF are situated 4-6 nm from the extracellular surface of the membrane. When cells were incubated for up to 30 min at 37 degrees C, this characteristic spatial relationship was observed in all uptake stages (surface clustering, endocytosis, and incorporation into multivesicular bodies), indicating that the hormone.receptor complex remains intact through these steps. However, when incubation was continued for periods sufficient to allow hormone degradation (30-60 min), pools of free ferritin were observed in lysosomes. In the presence of various amine inhibitors of hormone degradation, internalization and multivesicular body incorporation proceeded, but hormone.receptor degradation was blocked as evidenced by preservation of the ferritin-membrane relationship; i.e., no pools of free ferritin were seen after 60 min. These data provide morphological support for the hypothesis that down-regulation of surface receptors involves internalization of intact hormone.receptor complexes. In addition, we have developed a method for viewing the surface of intact cells en face, allowing closer scrutiny of the clustering of F-EGF.receptor complexes in the plane of the membrane prior to internalization. The particles in the F-EGF clusters observed by this method are spaced at 12 nm center-to-center, serving to set upper limits on the packing dimensions of the EGF.receptor complex.

Animals↗

PubMed1979

Pathophysiology of Cushing's disease.

The term Cushing's disease is applied to those cases of Cushing's syndrome in which hypercortisolism is secondary to inappropriate secretion of ACTH by the pituitary. Studies on control of ACTH secretion in these patients reveal: (a) that the episodic secretion of ACTH is similar to the normal; however, frequency and amplitude of the secretory episodes lack the normal circadian rhythm; (b) that ACTH release can be stimulated by vasopressin and metyrapone in a normal or above-normal manner; and (c) that it can be suppressed by large doses of corticosteroids. When the dynamic aspects of the ACTH response to corticosteroid administration are studied, it appears that the normally negative differential feedback mechanism is converted into a positive one, whereas the delayed, integral mechanism is undisturbed. Patients with Cushing's disease in the presence of obvious pituitary tumors cannot be distinguished from those without pituitary tumors by studying only the pituitary function. All these and other well-known facts would favor the concept that ACTH secretion in Cushing's disease is under hypothalamic control whether or not a pituitary tumor is present. Moreover, there are observations that suggest that brain centers superior to the hypophysiotropic area of the hypothalamus are involved in the pathophysiology of Cushing's disease. This concept has led to the discovery of neurotropic drugs that are able to induce complete remission of Cushing's syndrome in a cerain percentage of patients. In some patients with severe psychiatric diseases, neuroendocrine abnormalities are present that resemble closely those characteristic for Cushing's disease. With the most refined neuroradiological methods, pituitary microadenomas are demonstrable in approximately 70% of patients with Cushing's disease, and this number compares well with those of earlier autopsy findings (70 to 80%). In a small number of patients (4 to 10%), these tumors are large and can easily be detected by standard roentgenograms of the head. Recent studies on the frequency of these large tumors do not support the hypothesis that adrenalectomy accelerates the progression of these tumors. In this case the term "Nelson's syndrome" would be uncessary. It is established that complete cure of Cushing's disease can be obtained in most patients with selective removal of a microadenoma from the pituitary gland. The current experience with this microsurgical procedure caused a renewed interest in Cushing's original suggestion that the disease is primarily a pituitary disorder. However, there are already a number of enigmatic observations. Possibly, the recent ultrastructural studies using immunocytochemical methods will resolve some of these problems. At this moment it is impossible to decide whether Cushing's disease is primarily a CNS or a pituitary disorder, when all arguments for one or the other hypothesis are taken into account...

Adrenal Cortex Hormones↗