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PubMed2026

Hide and seek: de novo identification in sugar beet reveals impact of non-autonomous LTR retrotransposons.

Plant genomes are filled with retrotransposons and their derivatives, constantly undergoing sequence diversification and structural rearrangement. Among them, short, non-autonomous retrotransposons lack full coding capacity and often form subfamilies. As a result, non-autonomous retrotransposons are incompletely identified in most to all genome assemblies.Here, we capitalize on our comprehensive understanding of the transposable element (TE) landscape in sugar beet (Beta vulgaris) to assess the extent of the blind spot for non-autonomous long terminal repeat (LTR) retrotransposons. This use case serves to answer if all of these sequences are derivatives of easier-to-identify full-length elements or if there is more variability that is currently overlooked.For this we applied a semi-automated structural discovery workflow followed by in-depth manual verification to characterize non-autonomous LTR retrotransposons in sugar beet. We retrieve more than 100 non-autonomous LTR retrotransposon families that lack complete autonomous coding capacity, including canonical terminal-repeat retrotransposons in miniature (TRIMs), elongated non-coding derivatives and families retaining fragmented coding remnants. The identified families span a broad range, including elements exceeding 15,000 bp in length and display evidence for reshuffling and modular evolution. Only a subset of families could be confidently linked to autonomous retrotransposons, showing sequence diversification within the non-autonomous LTR retrotransposon fraction beyond the autonomous genomic templates.We highlight that a large fraction of non-autonomous LTR retrotransposons is incompletely recovered with the current TE identification workflows, even if the output is well-curated and condensed into TE libraries and suggest procedures to remedy this gap. This study gives a genome-wide view into the non-autonomous LTR retrotransposon landscape of a single plant genome and highlights the importance of structure-based approaches for their identification and classification.

LTR retrotransposons↗
PubMed1975

Estimation of non-autonomic and autonomic components of iliac bed vascular resistance in renal hypertensive rabbits.

Iliac bed vascular resistance (IVR) was measured before and after pharmacological block of the autonomic effectors in unanaesthetized renal hypertensive and normotensive rabbits with previously implanted Doppler flowmeters. This permitted partitioning the resting IVR into a non-autonomic component (ie, steady-state IVR after block) and an autonomic component (ie, resting IVR minus non-autonomic IVR). When IVR was measured at the same mean arterial pressure (MAP) before and after block in each animal, the increase in estimated non-autonomic IVR accounted entirely for the rise in resting IVR in renal hypertensive rabbits. However, if IVR measurements after block were made at a lower MAP than before block, the estimated non-autonomic and autonomic components were both significantly increased in renal hypertensive rabbits. It is concluded that in the latter experiment non-autonomic IVR in renal hypertension was underestimated, whilst the autonomic component was overestimated. The rise in non-autonomic IVR in renal hypertension was partly due to structural changes in the iliac bed, since IVR remained higher in hypertensive than in normotensive rabbits after abolishing smooth muscle tone with vasodilator drugs.

Animals↗
PubMed1976

Assessment of autonomic and non-autonomic components of resting hindlimb vascular resistance and reactivity to pressor substances in renal hypertensive rabbits.

1. Hindlimb vascular resistance (HVR) was measured before and after pharmacological autonomic blockade in unanesthetized renal cellophan-wrap hypertensive or normotensive rabbits with previously implanted Doppler ultrasonic flowmeters. 2. When the blood pressure was restored to resting values after autonomic block, the elevated resting HVR in the hypertensive rabbits was entirely accounted for by an increased non-autonomic component (i.e. HVR after block). If the pressure was not restored after block the autonomic component (i.e. resting HVR minus non-autonomic HVR) was overestimated and the non-autonomic component was underestimated. 3. During maximum vasodilatation the minimum HVR was significantly higher in the hypertensive rabbits than in the normotensive group, probably due to structural differences of resistance vessels. 4. Reactivity of the hindlimb bed to noradrenaline, angiotensin II and vasopressin injections was approximately twice as great in the hypertensive rabbits as in the sham-operated group, probably as a consequence of the structural changes.

Animals↗
PubMed1978

Role of autonomic and non-autonomic circulatory components in borderline hypertension in young men.

The role of autonomic nervous system and non-autonomic components in hemodynamic abnormalities of young patients with borderline hypertension was examined by comparing the effects of sequential pharmacological autonomic blockade on hemodynamics between 8 patients with borderline hypertension (mean age 20.0 +/- 0.2) and 10 normotensive subjects (mean age 19.3 +/- 0.2). Propranolol (0.2 mg/Kg), atropine (0.04 mg/Kg), and phenotolamine (10 or 15 mg) were given intravenously in that order to produce "total" autonomic blockade. Increased cardiac index, heart rate, and mean arterial blood pressure with normal peripheral vascular resistance were noted at rest in patients with borderline hypertension. Cardiac index and heart rate in patients with borderline hypertension were normalized by propranolol, but after "total" autonomic blockade mean arterial blood pressure and peripheral vascular resistance were higher in patients with borderline hypertension as compared to those in normotensive subjects. These results suggest that, although autonomic nervous system control of circulation is abnormal, non-autonomic components play an important role in maintaining increased peripheral vascular resistance in borderline hypertension in young men.

Adult↗
PubMed1979

Thyroid-stimulating immunoglobulins do not cause non-autonomous, autonomous, or toxic multinodular goitres.

Thyroid-stimulating immunoglobulins (TSIs) were measured by radioreceptor assay in serum from 51 patients with a multinodular goitre, divided into four groups according to thyroid function, and in 30 normal people. In 9 patients who were euthyroid and had non-autonomous thyroid function and in 6 patients who were hyperthyroid, TSI index was normal . Of 21 euthyroid patients with autonomous function only 2 had a slightly abnormal TSI index (66 in both, normal greater than or equal to 68). Another series of 15 clinically euthyroid patients also had a normal TSI index. These results suggest that TSIs do not contribute to the pathogenesis of multinodular goitre, as has been suggested by others.

Adult↗
PubMed1976

Autonomy of imagery and production of original verbal images.

90 college students (31 men and 59 women) were categorized as moderately autonomous, less autonomous (less highly controlled) and non-autonomous (high controlled) imagers according to the Gordon Test of Visual Imagery Control Moderately autonomous imagers produced significantly more original verbal images than less autonomous and non-autonomous imagers with less autonomous imagers scoring higher than non-autonomous imagers as measured by Onomatopoeia and Images. There were no significant sex main effects of interaction of autonomy of imagery level X sex.

Creativity↗
PubMed1992

Studies on the Mx transposable element system in maize recovered from X-irradiated stocks.

The unstable mutant bz-x3m arose in a plant subjected to X-irradiation. The element at the bronze locus is non-autonomous and recombination data indicate that an autonomous element is tightly linked. The autonomous element has been designated Mx (mobile element induced by X-rays) and the non-autonomous element, rMx (responder to Mx). Linkage data indicate that a second Mx lies near the end of the short arm of chromosome 9; in one plant, an Mx that is unlinked was detected. Distinguishing characteristics of bz-x3m are a large window of time in endosperm development during which somatic reversions can arise and a wide range in the frequency at which they occur; these features are heritable. With increasing doses of bz-x3m and Mx, the window expands and the frequency range increases. In kernels containing the bz-x3m allele and the tightly linked Mx, breakage occurs in chromosome 9 distal to the C locus, resulting in breakage-fusion-bridge patterns for endosperm markers that lie proximal to the break. The frequency of breaks and the developmental time at which they occur exhibit the same dosage effect as the somatic reversions of the bz-x3m allele. These observations suggest that an rMx (designated rMxBr) that causes chromosome breakage is positioned distal to the C locus. At the molecular level, the bz-x3m allele is associated with a 0.5 kb increase in fragment size in DNA samples digested with BglII, EcoRI, HindIII and PstI; in germinal revertants, the fragment size returns to that of the progenitor.

Alleles↗
PubMed2026

Spermatogenesis-specific Argonautes ALG-3/4 promote LEA-1 expression in oocytes.

Small interfering RNAs bound to Argonautes ALG-3 and ALG-4 ( ALG-3 /4) in spermatocytes regulate fertility and aging in C. elegans . ALG-3 /4 cell non-autonomously repress DAF-18 /PTEN in the oocyte, thereby limiting the activity of DAF-16 /FOXO and longevity. We find that the DAF-16 and ALG-3 /4 target gene lea-1 is downregulated in precursor germ cells and oocytes of alg-3 /4 mutants while being upregulated in age-1 ( hx546 ) PI3K mutants, where DAF-16 is activated. The downregulation of lea-1 in alg-3 /4 mutants is inherited, unlike the elevation in DAF-18 levels. We therefore propose that ALG-3 /4 regulate LEA-1 and DAF-18 through distinct non-autonomous mechanisms.

Journal Article↗
PubMed1975

Phenogenetics of the eyeless-dominant mutant of Drosophila melanogaster.

The eyeless-Dominant (eyD) mutation is a fourth chromosome insertional translocation which affects the eyes, antennae, ocelli, and sexcombs when heterozygous but is a larval-pupal lethal when homozygous. By use of a crowding technique, it was possible to separate eyD homozygotes and heterozygotes with 100% accuracy at an early stage of larval development. Under these conditions, the eyD homozygotes had a biphasic lethal period since 45% died as first or second instar larvae and 55% died as pupae. The eyDleyD pupal lethal, isolated by this technique, was able to form all the adult structures with the exception of the eye-antennal disc derivatives. The brain was present but abnormal. In testing the competence of the eyDleyD larval eye discs by means of transplantation experiments, it has been demonstrated that the mutant discs develop non-autonomously. Histological studies have revealed the existence of neurological defects in both eyD heterozygotes and homozygotes. The eyDleyD lethal larvae lacked detectable optic formation centers and showed an extreme reduction in the number of cells present in the cortex of the brain. The ey"dleyD lethal pupae possessed partial formation centers and also had severe reduction in the number of cortical cells. The eyD heterozygotes possessed normal appearing formation centers but they did exhibit a moderate reduction in the number of their cortical cells as compared to wild-type. These studies have shown that there is a direct correlation between the extent of neurological damage and the time of developmental arrest. It appears that the eyD mutation must adversely affect the neuroblasts at a very early stage of development. As a working hypothesis, it is suggested that the eyD mutation operates via the same basic mechanism of cell death in heterozygous and homozygous animals.

Animals↗
PubMed1992

Petunia plants escape from negative selection against a transgene by silencing the foreign DNA via methylation.

Transgenic Petunia hybrida clones harbouring the T-DNA gene 2 of Agrobacterium tumefaciens were used to test a strategy for the trapping of plant transposable elements. In the Petunia line used, floral variegation is due to the presence of the non-autonomous transposable element dTph1 at the An1 locus. The gene 2 product converts the auxin precursor indole-3-acetamide and its analogue 1-naphthalene acetamide into the active auxins indole-3-acetic acid and 1-naphthalene acetic acid. Plant cells that express gene 2 can use a low concentration of the precursors as auxins and become sensitive to the toxicity of high concentrations of these compounds. By selecting protoplast-derived microcalli or seedlings able to grow on medium with high precursor concentrations, variant plants were obtained in which gene 2 was no longer expressed. Southern analysis, using gene 2-specific probes, revealed that in one variant the T-DNA was deleted. For 30 other variants no alteration in gene 2 structure was observed, indicating that transposable element insertion was not responsible for the inactivation of gene 2. Analysis with restriction enzymes allowing discrimination between methylated or non-methylated DNA sequences showed that the inactivated gene 2 sequences were methylated. Addition of the in vivo methylation inhibitor 5-azacytidine to the medium led to reactivation of gene 2 expression in some of the variants. These observations demonstrated that reversible DNA methylation was the main cause of silencing of gene 2 in this system.

Agrobacterium tumefaciens↗
PubMed1979

Multiple system atrophy with autonomic failure: clinical, histological and neurochemical observations on four cases.

Four cases of progressive autonomic failure are described, in all of which there were additional non-autonomic neurological abnormalities, including pyramidal, extra-pyramidal and cerebellar features. Histological examination revealed cell degeneration in the substantia nigra, putamen and intermediolateral columns of the spinal cord as a common pathological finding. In addition, 3 cases showed loss of Purkinje cells in the cerebellum and degeneration of pontine nuclei and inferior olivary nuclei. In one case there was cell loss from the locus coeruleus, caudate nucleus, vestibular nuclei and dorsal vagal nuclei. These were, therefore, cases of multiple system atrophy. Neurochemically, a common feature was a profound depletion in dopamine and noradrenaline from brain regions which are normally rich in these catecholamines. Central cholinergic systems appeared to be involved also, but to a variable degree.

Aged↗
PubMed1976

Valsalva vasoconstrictor reflex in human hypertension in after beta-adrenoreceptor blockade in conscious rabbits.

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (SEM 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.

Adrenergic beta-Antagonists↗
PubMed2025

Spatially ordered zygotic genome activation fulfills embryo quality control.

Early embryo development features autonomous, maternally-driven cell divisions that self- organize the multicellular blastula or blastocyst tissue. Maternal control cedes to the zygote starting with the onset of widespread zygotic genome activation (ZGA), which is essential for subsequent cell fate determination and morphogenesis. Intriguingly, although the onset of ZGA is highly regulated at the level of an embryo, it can be non-homogenous and precisely patterned at the single-cell level. We previously demonstrated a stereotyped spatial and temporal ordering of ZGA in a model vertebrate embryo. Unknown, however, was whether this precise ZGA patterning was required for development. To address this fundamental question, we devised a strategy to spatially control cell divisions in the embryo that perturb blastula embryo organization. We demonstrate the feasibility of spatially inverting the cell size pattern of embryos and find that these inverted embryos undergo a flipped pattern of ZGA. Mispatterned ZGA along the animal-vegetal axis causes embryo apoptosis, revealing that gastrula embryos have a built-in quality control system to sense inappropriate ZGA patterning, including regional defects in transcriptional onset. The quality control response is non-autonomous which may depend on anti-apoptotic signals that repress cell death outside of the animal hemisphere. These results reveal the requirement of properly patterned ZGA for normal development and the existence of an embryo quality control response exquisitely tuned to the spatial and temporal ordering of genome activation and zygotic gene expression.

Journal Article↗