scholarly journals Establishing the role of SINE proteins in regulating stomatal dynamics in Arabidopsis thaliana

2019 ◽  
Author(s):  
Alecia Biel ◽  
Morgan Moser ◽  
Iris Meier
Keyword(s):  
Nuclear Envelope ◽  
Stomatal Closure ◽  
Large Degree ◽  
Stress Hormone ◽  
Linc Complex ◽  
Biotic And Abiotic Stresses ◽  
Actin Reorganization ◽  
Stomatal Regulation ◽  
Opening And Closing

AbstractStomatal movement, which regulates gas exchange in plants, is controlled by a variety of environmental factors, including biotic and abiotic stresses. The stress hormone ABA initiates a signaling cascade, which leads to increased H2O2 and Ca2+ levels and F-actin reorganization, but the mechanism of, and connection between, these events is unclear. SINE1, an outer nuclear envelope component of a plant Linker of Nucleoskeleton and Cytoskeleton (LINC) complex, associates with F-actin and is, along with its paralog SINE2, expressed in guard cells. Here, we have determined that Arabidopsis SINE1 and SINE2 play an important role in stomatal regulation. We show that SINE1 and SINE2 are required for stomatal opening and closing. Loss of SINE1 or SINE2 results in ABA hyposensitivity and impaired stomatal dynamics but does not affect stomatal closure induced by the bacterial elicitor flg22. The ABA-induced stomatal closure phenotype is, in part, attributed to impairments in Ca2+ and F-actin regulation. Together, the data suggest that SINE1 and SINE2 act downstream of ABA but upstream of Ca2+ and F-actin. While there is a large degree of functional overlap between the two proteins, there are also critical differences. Our study makes an unanticipated connection between stomatal regulation and a novel class of nuclear envelope proteins, and adds two new players to the increasingly complex system of guard cell regulation.

scholarly journals Mutant lamins cause nuclear envelope rupture and DNA damage in skeletal muscle cells

2018 ◽  
Author(s):  
Ashley J. Earle ◽  
Tyler J. Kirby ◽  
Gregory R. Fedorchak ◽  
Philipp Isermann ◽  
Jineet Patel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Dna Damage ◽  
Muscular Dystrophy ◽  
Nuclear Envelope ◽  
Mouse Models ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Causative Role ◽  
Linc Complex

ABSTRACTMutations in the human LMNA gene, which encodes the nuclear envelope (NE) proteins lamins A and C, cause autosomal dominant Emery-Dreifuss muscular dystrophy, congenital muscular dystrophy, limb-girdle muscular dystrophy, and other diseases collectively known as laminopathies. The molecular mechanisms responsible for these diseases remain incompletely understood, but the muscle-specific defects suggest that mutations may render nuclei more susceptible to mechanical stress. Using three mouse models of muscle laminopathies, we found that Lmna mutations caused extensive NE abnormalities, consisting of chromatin protrusions into the cytoplasm and transient rupture of the NE in skeletal muscle cells. NE damage was associated with DNA damage, activation of DNA damage response pathways, and reduced viability. Intriguingly, NE damage resulted from nuclear migration in maturing skeletal muscle cells, rather than actomyosin contractility. NE damage and DNA damage was reduced by either depletion of kinesin-1 or disruption of the Linker of Nucleoskeleton and Cytoskeleton (LINC) complex. LINC complex disruption rescued myofiber function and viability in Lmna mutant myofibers, indicating that the myofiber dysfunction is the result of mechanically induced NE damage. The extent of NE damage and DNA damage in Lmna mouse models correlated with the disease onset and severity in vivo. Moreover, inducing DNA damage in wild-type muscle cells was sufficient to phenocopy the reduced cell viability of lamin A/C-deficient muscle cells, suggesting a causative role of DNA damage in disease pathogenesis. Corroborating the mouse model data, muscle biopsies from patients with LMNA muscular dystrophy revealed significant DNA damage compared to age-matched controls, particularly in severe cases of the disease. Taken together, these findings point to a new and important role of DNA damage as a pathogenic contributor for LMNA skeletal muscle diseases.

scholarly journals The testis-specific LINC component SUN3 is essential for sperm head shaping during mouse spermiogenesis

2020 ◽  
Vol 295 (19) ◽  
pp. 6289-6298 ◽  
Author(s):  
Qian Gao ◽  
Ranjha Khan ◽  
Changping Yu ◽  
Manfred Alsheimer ◽  
Xiaohua Jiang ◽  
...  
Keyword(s):  
Nuclear Envelope ◽  
Male Fertility ◽  
Sperm Head ◽  
Mechanical Forces ◽  
Linc Complex ◽  
Sperm Counts ◽  
Sperm Nuclei ◽  
Sun Domain ◽  
Underlying Pathology

Sperm head shaping is a key event in spermiogenesis and is tightly controlled via the acrosome–manchette network. Linker of nucleoskeleton and cytoskeleton (LINC) complexes consist of Sad1 and UNC84 domain–containing (SUN) and Klarsicht/ANC-1/Syne-1 homology (KASH) domain proteins and form conserved nuclear envelope bridges implicated in transducing mechanical forces from the manchette to sculpt sperm nuclei into a hook-like shape. However, the role of LINC complexes in sperm head shaping is still poorly understood. Here we assessed the role of SUN3, a testis-specific LINC component harboring a conserved SUN domain, in spermiogenesis. We show that CRISPR/Cas9-generated Sun3 knockout male mice are infertile, displaying drastically reduced sperm counts and a globozoospermia-like phenotype, including a missing, mislocalized, or fragmented acrosome, as well as multiple defects in sperm flagella. Further examination revealed that the sperm head abnormalities are apparent at step 9 and that the sperm nuclei fail to elongate because of the absence of manchette microtubules and perinuclear rings. These observations indicate that Sun3 deletion likely impairs the ability of the LINC complex to transduce the cytoskeletal force to the nuclear envelope, required for sperm head elongation. We also found that SUN3 interacts with SUN4 in mouse testes and that the level of SUN4 proteins is drastically reduced in Sun3-null mice. Altogether, our results indicate that SUN3 is essential for sperm head shaping and male fertility, providing molecular clues regarding the underlying pathology of the globozoospermia-like phenotype.

scholarly journals An R2R3-type myeloblastosis transcription factor MYB103 is involved in phosphorus remobilization

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Fangwei Yu ◽  
Shenyun Wang ◽  
Wei Zhang ◽  
Hong Wang ◽  
Li Yu ◽  
...  
Keyword(s):  
Cell Wall ◽  
Transcription Factor ◽  
Abiotic Stresses ◽  
Myb Transcription Factor ◽  
Ethylene Signaling ◽  
Biotic And Abiotic Stresses ◽  
P Deficiency ◽  
P Concentration ◽  
Increased Sensitivity

Abstract The members of myeloblastosis transcription factor (MYB TF) family are involved in the regulation of biotic and abiotic stresses in plants. However, the role of MYB TF in phosphorus remobilization remains largely unexplored. In the present study, we show that an R2R3 type MYB transcription factor, MYB103, is involved in phosphorus (P) remobilization. MYB103 was remarkably induced by P deficiency in cabbage (Brassica oleracea var. capitata L.). As cabbage lacks the proper mutant for elucidating the mechanism of MYB103 in P deficiency, another member of the crucifer family, Arabidopsis thaliana was chosen for further study. The transcript of its homologue AtMYB103 was also elevated in response to P deficiency in A. thaliana, while disruption of AtMYB103 (myb103) exhibited increased sensitivity to P deficiency, accompanied with decreased tissue biomass and soluble P concentration. Furthermore, AtMYB103 was involved in the P reutilization from cell wall, as less P was released from the cell wall in myb103 than in wildtype, coinciding with the reduction of ethylene production. Taken together, our results uncover an important role of MYB103 in the P remobilization, presumably through ethylene signaling.

scholarly journals LINCking the Nuclear Envelope to Sperm Architecture

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 658
Author(s):  
Francesco Manfrevola ◽  
Florian Guillou ◽  
Silvia Fasano ◽  
Riccardo Pierantoni ◽  
Rosanna Chianese
Keyword(s):  
Nuclear Envelope ◽  
Male Fertility ◽  
Nuclear Architecture ◽  
Sperm Cells ◽  
Bridge Structure ◽  
Linc Complex ◽  
Head Formation ◽  
Morphological Maturation ◽  
Integral Proteins ◽  
Sun Domain

Nuclear architecture undergoes an extensive remodeling during spermatogenesis, especially at levels of spermatocytes (SPC) and spermatids (SPT). Interestingly, typical events of spermiogenesis, such as nuclear elongation, acrosome biogenesis, and flagellum formation, need a functional cooperation between proteins of the nuclear envelope and acroplaxome/manchette structures. In addition, nuclear envelope plays a key role in chromosome distribution. In this scenario, special attention has been focused on the LINC (linker of nucleoskeleton and cytoskeleton) complex, a nuclear envelope-bridge structure involved in the connection of the nucleoskeleton to the cytoskeleton, governing mechanotransduction. It includes two integral proteins: KASH- and SUN-domain proteins, on the outer (ONM) and inner (INM) nuclear membrane, respectively. The LINC complex is involved in several functions fundamental to the correct development of sperm cells such as head formation and head to tail connection, and, therefore, it seems to be important in determining male fertility. This review provides a global overview of the main LINC complex components, with a special attention to their subcellular localization in sperm cells, their roles in the regulation of sperm morphological maturation, and, lastly, LINC complex alterations associated to male infertility.

Inhibition of cambial activity in Abies balsamea by internal water stress: role of abscisic acid

1975 ◽  
Vol 53 (24) ◽  
pp. 3041-3050 ◽  
Author(s):  
C. H. A. Little
Keyword(s):  
Abscisic Acid ◽  
Water Stress ◽  
Indoleacetic Acid ◽  
Stomatal Closure ◽  
Abies Balsamea ◽  
Cambial Activity ◽  
Inhibitory Effect ◽  
Internal Water ◽  
Endogenous Aba

In experiments with attached and detached shoots of balsam fir, Abies balsamea L., synthetic (±)abscisic acid (ABA) (1) reduced photosynthesis and transpiration by inducing stomatal closure, (2) inhibited indoleacetic acid (IAA) - induced cambial activity in photosynthesizing and non-photosynthesizing shoots, and (3) inhibited the basipetal movement of [14C]IAA. Neither gibberellic acid nor kinetin counteracted the inhibitory effect of (±)ABA on IAA-induced cambial activity. In addition it was demonstrated that increasing the internal water stress increased the level of endogenous ABA in the phloem–cambial region of bark peelings and decreased the basipetal movement of [14C]IAA through branch sections. On the basis of these findings it is proposed that internal water stress inhibits cambial activity, partly through increasing the level of ABA; the ABA acts to decrease the provision of carbohydrates and auxin that are required for cambial growth.

scholarly journals Sigma-1 receptor mediates cocaine-induced transcriptional regulation by recruiting chromatin-remodeling factors at the nuclear envelope

2015 ◽  
Vol 112 (47) ◽  
pp. E6562-E6570 ◽  
Author(s):  
Shang-Yi A. Tsai ◽  
Jian-Ying Chuang ◽  
Meng-Shan Tsai ◽  
Xiao-fei Wang ◽  
Zheng-Xiong Xi ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Nuclear Envelope ◽  
Chromatin Remodeling ◽  
Behavioral Sensitization ◽  
Specific Protein ◽  
Cellular Regulation ◽  
Sigma 1 Receptor ◽  
Withdrawal Treatment ◽  
Sigma 1

The sigma-1 receptor (Sig-1R) chaperone at the endoplasmic reticulum (ER) plays important roles in cellular regulation. Here we found a new function of Sig-1R, in that it translocates from the ER to the nuclear envelope (NE) to recruit chromatin-remodeling molecules and regulate the gene transcription thereof. Sig-1Rs mainly reside at the ER–mitochondrion interface. However, on stimulation by agonists such as cocaine, Sig-1Rs translocate from ER to the NE, where Sig-1Rs bind NE protein emerin and recruit chromatin-remodeling molecules, including lamin A/C, barrier-to-autointegration factor (BAF), and histone deacetylase (HDAC), to form a complex with the gene repressor specific protein 3 (Sp3). Knockdown of Sig-1Rs attenuates the complex formation. Cocaine was found to suppress the gene expression of monoamine oxidase B (MAOB) in the brain of wild-type but not Sig-1R knockout mouse. A single dose of cocaine (20 mg/kg) in rats suppresses the level of MAOB at nuclear accumbens without affecting the level of dopamine transporter. Daily injections of cocaine in rats caused behavioral sensitization. Withdrawal from cocaine in cocaine-sensitized rats induced an apparent time-dependent rebound of the MAOB protein level to about 200% over control on day 14 after withdrawal. Treatment of cocaine-withdrawn rats with the MAOB inhibitor deprenyl completely alleviated the behavioral sensitization to cocaine. Our results demonstrate a role of Sig-1R in transcriptional regulation and suggest cocaine may work through this newly discovered genomic action to achieve its addictive action. Results also suggest the MAOB inhibitor deprenyl as a therapeutic agent to block certain actions of cocaine during withdrawal.

scholarly journals Hormonal and Hydroxycinnamic Acids Profiles in Banana Leaves in Response to Various Periods of Water Stress

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jalel Mahouachi ◽  
María F. López-Climent ◽  
Aurelio Gómez-Cadenas
Keyword(s):  
Water Stress ◽  
Leaf Gas Exchange ◽  
Stomatal Closure ◽  
Photosynthetic Performance ◽  
Hydroxycinnamic Acids ◽  
Cinnamic Acids ◽  
Gas Exchange Parameters ◽  
Banana Leaves ◽  
Indole 3 Acetic Acid

The pattern of change in the endogenous levels of several plant hormones and hydroxycinnamic acids in addition to growth and photosynthetic performance was investigated in banana plants (Musa acuminatacv. “Grand Nain”) subjected to various cycles of drought. Water stress was imposed by withholding irrigation for six periods with subsequent rehydration. Data showed an increase in abscisic acid (ABA) and indole-3-acetic acid (IAA) levels, a transient increase in salicylic acid (SA) concentration, and no changes in jasmonic acid (JA) after each period of drought. Moreover, the levels of ferulic (FA) and cinnamic acids (CA) were increased, and plant growth and leaf gas exchange parameters were decreased by drought conditions. Overall, data suggest an involvement of hormones and hydroxycinnamic acids in plant avoidance of tissue dehydration. The increase in IAA concentration might alleviate the senescence of survival leaves and maintained cell elongation, and the accumulation of FA and CA could play a key role as a mechanism of photoprotection through leaf folding, contributing to the effect of ABA on inducing stomatal closure. Data also suggest that the role of SA similarly to JA might be limited to a transient and rapid increase at the onset of the first period of stress.

scholarly journals Calcium Signaling in Plant Programmed Cell Death

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1089
Author(s):  
Huimin Ren ◽  
Xiaohong Zhao ◽  
Wenjie Li ◽  
Jamshaid Hussain ◽  
Guoning Qi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Abiotic Stresses ◽  
Animal Studies ◽  
Future Research ◽  
Significant Progress ◽  
Biotic And Abiotic Stresses ◽  
Stress Perception ◽  
The Past

Programmed cell death (PCD) is a process intended for the maintenance of cellular homeostasis by eliminating old, damaged, or unwanted cells. In plants, PCD takes place during developmental processes and in response to biotic and abiotic stresses. In contrast to the field of animal studies, PCD is not well understood in plants. Calcium (Ca2+) is a universal cell signaling entity and regulates numerous physiological activities across all the kingdoms of life. The cytosolic increase in Ca2+ is a prerequisite for the induction of PCD in plants. Although over the past years, we have witnessed significant progress in understanding the role of Ca2+ in the regulation of PCD, it is still unclear how the upstream stress perception leads to the Ca2+ elevation and how the signal is further propagated to result in the onset of PCD. In this review article, we discuss recent advancements in the field, and compare the role of Ca2+ signaling in PCD in biotic and abiotic stresses. Moreover, we discuss the upstream and downstream components of Ca2+ signaling and its crosstalk with other signaling pathways in PCD. The review is expected to provide new insights into the role of Ca2+ signaling in PCD and to identify gaps for future research efforts.

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