共查询到20条相似文献,搜索用时 15 毫秒
1.
Helene M. Langevin Kirsten N. Storch Robert R. Snapp Nicole A. Bouffard Gary J. Badger Alan K. Howe Douglas J. Taatjes 《Histochemistry and cell biology》2010,133(4):405-415
Studies in cultured cells have shown that nuclear shape is an important factor influencing nuclear function, and that mechanical
forces applied to the cell can directly affect nuclear shape. In a previous study, we demonstrated that stretching of whole
mouse subcutaneous tissue causes dynamic cytoskeletal remodeling with perinuclear redistribution of α-actin in fibroblasts
within the tissue. We have further shown that the nuclei of these fibroblasts have deep invaginations containing α-actin.
In the current study, we hypothesized that tissue stretch would cause nuclear remodeling with a reduced amount of nuclear
invagination, measurable as a change in nuclear concavity. Subcutaneous areolar connective tissue samples were excised from
28 mice and randomized to either tissue stretch or no stretch for 30 min, then examined with histochemistry and confocal microscopy.
In stretched tissue (vs. non-stretched), fibroblast nuclei had a larger cross-sectional area (P < 0.001), smaller thickness (P < 0.03) in the plane of the tissue, and smaller relative concavity (P < 0.005) indicating an increase in nuclear convexity. The stretch-induced loss of invaginations may have important influences
on gene expression, RNA trafficking and/or cell differentiation. 相似文献
2.
Fibroblast spreading induced by connective tissue stretch involves intracellular redistribution of α- and β-actin 总被引:3,自引:3,他引:0
Langevin HM Storch KN Cipolla MJ White SL Buttolph TR Taatjes DJ 《Histochemistry and cell biology》2006,125(5):487-495
Mechanical stretching of connective tissue occurs with normal movement and postural changes, as well as treatments including physical therapy, massage and acupuncture. Connective tissue fibroblasts were recently shown to respond actively to short-term mechanical stretch (minutes to hours) with reversible cytoskeletal remodeling, characterized by extensive cell spreading and lamellipodia formation. In this study, we have examined the effect of tissue stretch on the distribution of α- and β-actin in subcutaneous tissue fibroblasts ex vivo. Normal fibroblasts uniformly exhibited α-smooth muscle actin (α-SMA) immunoreactivity. Unlike cultured fibroblasts and smooth muscle cells, α-SMA in these fibroblasts was not in F-actin form (indicated by lack of phalloidin co-localization) nor was it organized into distinct stress fibers. The lack of stress fibers and fibronexus was confirmed by electron microscopy, indicating that these cells were not myofibroblasts. In unstretched tissue, the pattern of α-actin was diffuse and granular. With tissue stretch (30 min), α-actin formed a star-shaped pattern centered on the nucleus, while β-actin extended throughout the cytoplasm including lamellipodia and cell cortex. This dual response pattern of α- and β-actin may be an important component of cellular mechanotransduction mechanisms relevant to physiologic and therapeutic mechanical forces applied to connective tissue. 相似文献
3.
Nakatani T Honda E Hayakawa S Sato M Satoh K Kudo M Munakata H 《Molecular and cellular biochemistry》2008,308(1-2):201-207
Myofibroblasts are metabolically and morphologically distinctive fibroblasts expressing α-smooth muscle actin (α-SMA), and
their activation plays a key role in development of the fibrotic response. In an activated state, myofibroblasts cease to
proliferate and start to synthesize large amounts of extracellular component proteins. The expression of α-SMA correlates
with the activation of myofibroblasts. Decorin, a member of the small leucine-rich proteoglycan gene family, has been implicated
in the negative control of cell proliferation primarily by upregulating the expression of p21, a potent inhibitor of cyclin-dependent
kinase. In order to examine the effect of decorin on myofibroblast cell growth, we rendered a human lung myofibroblast cell
line, MRC-5, quiescent by either cell–cell contact or serum starvation, and examined the relationship between decorin and
α-SMA expression in these cells. The expression of decorin in cells made quiescent by serum starvation was lower than that
in cells made quiescent by cell–cell contact. In contrast, the expression of α-SMA in cells made quiescent by cell–cell contact
was lower than that in cells made quiescent by serum starvation. Furthermore, forced expression of decorin was accompanied
by a suppression of α-SMA expression, whereas knocking down of decorin expression by RNA interference increased the expression
of α-SMA. 相似文献
4.
Mizuho Tamura Reiko Aizawa Masatoshi Hori Hiroshi Ozaki 《Histochemistry and cell biology》2009,131(4):483-490
Adenine phosphoribosyltransferase deficiency in mice or an excessive oral intake of adenine leads to the accumulation of 2,8-dihydroxyadenine
(DHA) in renal tubules and that causes progressive renal dysfunction accompanied by interstitial fibrosis. However, the precise
mechanism responsible for DHA-induced progressive fibrosis is not fully understood. The present study investigates the possible
involvement of monocytes/macrophages in the progressive fibrosis induced by feeding adenine to mice. Urinary calculi were
deposited in tubules on day 7 after the initiation of adenine feeding. Elevation of the serum creatinine level and loss of
body weight were observed in a time-dependent manner, suggesting the development of typical renal dysfunction induced by the
adenine feeding. In renal tissue, mRNA expression of MCP-1, MIP-1α, RANTES, IL-1β, CCR2, TGF-β, α-smooth muscle actin (α-SMA)
and collagen 1a1 was increased in parallel. Along with the increased expression of these genes, a remarkable infiltration
of macrophages into the tubulointerstitial area was observed in a time-dependent manner. In addition, in the tubulointerstitial
area, α-SMA positive fibroblasts were increased in parallel with collagen deposition. These results suggest that the excessive
consumption of adenine leads to progressive renal dysfunction in mice. We speculate that the accumulation of DHA in tubules
might stimulate epithelium to produce MCP-1 and that profibrogenic TGF-β produced by infiltrated macrophages might stimulate
interstitial fibroblasts to produce collagen. These results indicate that macrophage infiltration is one of the triggers that
initiates interstitial fibroblast activation and collagen deposition followed by renal dysfunction. 相似文献
5.
6.
Rishikof DC Lucey EC Kuang PP Snider GL Goldstein RH 《Histochemistry and cell biology》2006,125(5):527-534
The repair of alveolar structures following endotracheal administration of porcine pancreatic elastase (PPE) to mice involves the coordinated deposition of new matrix elements. We determined the induction of the myofibroblast phenotype following elastolytic injury to mouse lung by examining the expression of α-smooth muscle actin (α-SMA) by immunohistochemistry. We also examined elastin and α1(I) collagen mRNA expression by in situ hybridization. Changes in airspace dimensions were assessed by determining mean linear intercept. In untreated mice, α-SMA was localized to vascular structures and large airways, with no detectable expression in alveolar units. PPE induced α-SMA expression in damaged areas surrounding large vessels, in septal remnants, and in the opening ring of alveolar ducts. Elastin and α1(I) collagen mRNA expression were up-regulated in residual alveolar structures and septal walls. PPE dose-response studies indicated that α1(I) collagen and elastin mRNA expression were not induced in areas of normal lung adjacent to damaged lung. The administration of low dose PPE resulted in increased α-SMA protein and elastin mRNA expression in the cells comprising the opening ring of alveolar ducts. Our data suggest that repair mechanisms following elastolytic injury are confined to overtly damaged alveolar structures and involve the induction of the myofibroblast phenotype. 相似文献
7.
The origin of fibrotic cells within connective tissue is unclear. For example, the extent to which microvascular pericytes
contribute to the number of myofibroblasts present in dermal fibrosis in uncertain. Connective tissue growth factor (CTGF/CCN2)
is a marker and mediator of fibrosis. In this report, we use an antibody recognizing CCN2 to assess the cell types in mouse
dermis which express CCN2 in the bleomycin model of skin scleroderma. Control (PBS injected) and fibrotic (bleomycin-injected)
dermis was examined for CCN2, α-smooth muscle actin (α-SMA) (to detect myofibroblasts), and NG2 (to detect pericytes) expression.
Consistent with previously published data, CCN2 expression was largely absent in the dermis of control mice. However, upon
exposure to bleomycin, CCN2 was observed in the dermis. Cells that expressed CCN2 were α−SMA-expressing myofibroblasts. Approximately
85% of myofibroblasts were NG2-positive, CCN2-expressing pericytes, indicating that pericytes significantly contributed to
the presence of myofibroblasts in sclerotic dermis. Thus CCN2 is induced in fibrotic skin, correlating with the induction
of myofibroblast induction. Moreover, CCN2-expressing pericytes significantly contribute to the appearance of myofibroblasts
in bleomycin-induced skin scleroderma. 相似文献
8.
Schneider M Andersen DC Silahtaroglu A Lyngbæk S Kauppinen S Hansen JL Sheikh SP 《Journal of molecular histology》2011,42(4):289-299
MicroRNAs (miRNAs) regulate gene expression by mediating translational repression or mRNA degradation of their targets, and
several miRNAs control developmental decisions through embryogenesis. In the developing heart, miRNA targets comprise key
players mediating cardiac lineage determination. However, although several miRNAs have been identified as differentially regulated
during cardiac development and disease, their distinct cell-specific localization remains largely undetermined, likely owing
to a lack of adequate methods. We therefore report the development of a markedly improved approach combining fluorescence-based
miRNA-in situ hybridization (miRNA-ISH) with immunohistochemistry (IHC). We have applied this protocol to differentiating
embryoid bodies (EBs) as well as embryonic and adult mouse hearts, to detect miRNAs that were upregulated during EB cardiomyogenesis,
as determined by array-based miRNA expression profiling. In this manner, we found specific co-localization of miR-1 to myosin
positive cells (cardiomyocytes) of EBs, developing and mature hearts. In contrast, miR-125b and -199a did not localize to
cardiomyocytes, as previously suggested for miR-199a, but were rather expressed in connective tissue cells of the heart. More
specifically, by co-staining with α-smooth muscle actin (α-SMA) and collagen-I, we found that miR-125b and -199a localize
to perivascular α-SMA− stromal cells. Our approach thus proved valid for determining cell-specific localization of miRNAs, and the findings we present
highlight the importance of determining exact cell-specific localization of miRNAs by sequential miRNA-ISH and IHC in studies
aiming at understanding the role of miRNAs and their targets. This approach will hopefully aid in identifying relevant miRNA
targets of both the heart and other organs. 相似文献
9.
Hiroyuki Kamiguchi Kazunari Yoshida Hirooki Wakamoto Makoto Inaba Hikaru Sasaki Mitsuhiro Otani Shigeo Toya 《Neurochemical research》1996,21(6):701-706
Cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and epidermal growth factor (EGF) are probable factors
responsible for up-regulation of basic fibroblast growth factor (bFGF) expression in reactive astrocytes following brain damage,
however the effect of these cytokines on the expression of each bFGF-isoform has not been elucidated. Western biot analysis
revealed the expression of 18, 22 and 24-kD bFGF isoforms in cultured rat hippocampal astrocytes, and the expression of high
molecular weight (HMW)-isoforms (22 and 24-kD isoforms) but not of 18-kD isoform was selectively increased by cytokines. Immunofluorescent
analysis demonstrated that bFGF content in the cytoplasm of astrocytes is initially increased by cytokines followed by nuclear
targeting and localization in agreement with the previous evidence that HMW-isoforms possess a nuclear targeting signal. The
present results suggest the important role of HMW-bFGF isoforms in the response of nervous tissue to injury. 相似文献
10.
Regulation on the function of the hepatic stellate cells (HSCs) is one of the proposed therapeutic approaches to liver fibrosis.
In the present study, we examined the in vitro and in vivo effects of CPU-II2, a novel synthetic oleanolic acid (OLA) derivative with nitrate, on hepatic fibrosis. This compound alleviated CCl4-induced hepatic fibrosis in mice with a decrease in hepatic hydroxyproline (Hyp) content and histological changes. CPU-II2 also attenuated the mRNA expression of α-smooth muscle actin (α-SMA) and tissue inhibitor of metalloproteinase type 1 (TIMP-1) induced by CCl4 in mice and reduced both mRNA and protein levels of α-SMA in HSC-T6 cells. Interestingly, CPU-II2 did not affect the survival of HSC-T6 cells but decreased the expression of procollagen-α1 (I) in HSC-T6 cells through down-regulating
the phosphorylation of p38 MAPK. Conclusion: CPU-II2 attenuates the development of liver fibrosis rather by regulating the function of HSCs through p38 MAPK pathway than by damaging
the stellate cells. 相似文献
11.
Yota Mizuno Mayu Suzuki Hiroki Nakagawa Nana Ninagawa Shigeko Torihashi 《Histochemistry and cell biology》2009,132(6):669-672
Among six actin isoforms, α-skeletal and α-cardiac actins have similar amino acid components and are highly conserved. Although
skeletal muscles essentially express α-skeletal actins in the adult tissue, α-cardiac isoform actin is prominent in the embryonic
muscle tissue. Switching of actin isoforms from α-cardiac to α-skeletal actin occurs during skeletal muscle differentiation.
The cardiac type α-actin is expressed in the regeneration and patho-physiological states of the skeletal muscles as well.
In the present study, we demonstrate the morphological switching of α-type actin isoforms from α-cardiac to α-skeletal actin
in vitro using mouse ES cells for the first time. Immunofluorescent double staining with two specific antibodies revealed
that α-cardiac actin appeared first in myoblasts. After cell fusion to form myotubes, the cardiac type actin decreased and
α-skeletal actin conversely increased. Finally, the α-skeletal isoform remained as a main actin component in the fully mature
skeletal muscle fibers. The exchange of isoforms is not directly linked to the sarcomere formation. As a result, ES cells
provide a useful in vitro system for exploring skeletal muscle differentiation. 相似文献
12.
13.
The behavior of fibroblasts on patterned substrates was examined in order to elucidate the role of dermal structure in wound
healing. Dermal fibroblasts were cultured on micro-patterned silicone elastomer substrates designed to enforce cell adhesion
only to fibronectin microdots. The morphology, expression of α-smooth muscle actin (α-SMA), proliferation, apoptotic cells,
and soluble collagen production of cells were measured. Cells grown on patterned substrates showed some signs of a scar-fibroblast
phenotype such as: elongated pseudopodia, enhanced expression of alpha smooth muscle actin (α-SMA), and increased collagen/pre-collagen,
in comparison to unpatterned controls. Cells also showed low proliferation rates and high apoptotic index. The results showed
that the microdot arrays, acting as a grid of limited focal adhesion sites, could force cells to adopt constrained morphologies
and limited adhesion areas, which affect the cytoskeleton, ultimately leading to expression of a scar-tissue fibroblast phenotype.
This study provides insight into the regulatory mechanisms of micro-topology on cell behavior in wound healing. 相似文献
14.
The effects of ACE inhibitor and angiotensin receptor blocker on clusterin and apoptosis in the kidney tissue of streptozotocin-diabetic rats 总被引:1,自引:0,他引:1
Our first aim was to determine the effects of secreted clusterin (sCLU) and nuclear clusterin (nCLU) in diabetic nephropathy.
We also aimed to investigate the post-effects of angiotensin II blockage treatment on clusterin expression and to compare
these with apoptosis. Five groups of Wistar albino rats were used: First group consisted of healthy controls; the second group
included the untreated STZ-diabetics; 30 days of irbesartan or perindopril treated STZ-diabetics formed the third and the
fourth groups, respectively; while the subjects receiving a combined treatment with irbesartan and perindopril for 30 days
consisted the fifth group. TUNEL method for apoptosis and immunohistochemical staining for TGF-β1, α-SMA, clusterin-β and
clusterin-α/β antibodies were performed. Apoptotic cells especially increased in the kidney tubuli of untreated diabetic group
and on the contrary, a significant decrease was observed in the group that received a combined drug treatment. While sCLU
was increased in the glomeruli and tubuli of the untreated diabetic group, it was decreased in all the treated groups. An
increase in the nCLU immunoreactivity was observed in the podocytes, mesangial cells, and the injured tubule cells of the
untreated diabetic group. nCLU immunopositive cells were decreased in all treated diabetic groups. In addition to this, the
distribution of nCLU was similar to the distribution of apoptotic cells in the diabetic groups. Our results indicate that
sCLU expression in diabetic nephropathy was induced due to renal tissue damage, and the nCLU expression increase in renal
tubuli was related to apoptosis. Although irbesartan and perindopril prevented further renal injury in diabetes, a combined
application of low-dose ACEI and AT1R blockers revealed more efficient measures, by means of renal damage prevention. 相似文献
15.
Brandon C Rindfleisch M Scott Brown John L VandeBerg Stephen H Munroe 《BMC molecular biology》2010,11(1):97
Background
Alternative processing of α-thyroid hormone receptor (TRα, NR1A1) mRNAs gives rise to two functionally antagonistic nuclear receptors: TRα1, the α-type receptor, and TRα2, a non-hormone binding variant that is found only in mammals. TRα2 shares an unusual antisense coding overlap with mRNA for Rev-erbα (NR1D1), another nuclear receptor protein. In this study we examine the structure and expression of these genes in the gray short-tailed opossum, Monodelphis domestica, in comparison with that of eutherian mammals and three other marsupial species, Didelphis virginiana, Potorous tridactylus and Macropus eugenii, in order to understand the evolution and regulatory role of this antisense overlap. 相似文献16.
Xu GP Li QQ Cao XX Chen Q Zhao ZH Diao ZQ Xu ZD 《Cellular & molecular biology letters》2007,12(3):457-472
The aim of this study was to investigate whether transforming growth factor-β1 (TGF-β1) could induce alveolar epithelial-mesenchymal
transition (EMT) in vitro, and whether Smad7 gene transfer could block this transition. We also aimed to elucidate the possible mechanisms of these
processes. The Smad7 gene was transfected to the rat type II alveolar epithelial cell line (RLE-6TN). Expression of the EMT-associated
markers was assayed by Western Blot and Real-time PCR. Morphological alterations were examined via phase-contrast microscope
and fluorescence microscope, while ultrastructural changes were examined via electron microscope. TGF-β1 treatment induced
a fibrotic phenotype of RLE-6TN with increased expression of fibronectin (FN), α-smooth muscle actin (α-SMA) and vimentin,
and decreased expression of E-cadherin (E-cad) and cytokeratin19 (CK19). After transfecting the RLE-6TN with the Smad7 gene,
the expression of the mesenchymal markers was downregulated while that of the epithelial markers was upregulated. TGF-β1 treatment
for 48 h resulted in the separation of RLE-6TN from one another and a change into elongated, myofibroblast-like cells. After
the RLE-6TN had been transfected with the Smad7 gene, TGF-β1 treatment had no effect on the morphology of the RLE-6TN. TGF-β1
treatment for 48 h resulted in an abundant expression of α-SMA in the RLE-6TN. If the RLE-6TN were transfected with the Smad7
gene, TGF-β1 treatment for 48 h could only induce a low level of α-SMA expression. Furthermore, TGF-β1 treatment for 12 h
resulted in the degeneration and swelling of the osmiophilic multilamellar bodies, which were the markers of type II alveolar
epithelial cells. TGF-β1 can induce alveolar epithelialmesenchymal transition in vitro, which is dependent on the Smads signaling pathway to a certain extent. Overexpression of the Smad7 gene can partially block
this process 相似文献
17.
Sergei Vyalov Alexis Desmoulière Giulio Gabbiani 《Virchows Archiv. B, Cell pathology including molecular pathology》1993,63(1):231-239
We have studied the formation of granulation tissue around osmotic minipumps delivering granulocyte macrophage-colony stimulating
factor (GM-CSF) chronologically in the rat using electron microscopy and immunohistochemistry at the light and electron microscopic
levels, with specific antibodies against α-smooth muscle (SM) actin and rat macrophages. At 2 and 3 days after pump implantation,
GM-CSF application produced an extensive inflammatory reaction characterized by edema and the accumulation of polymorphonuclear
cells and macrophages. Gradually, polymorphonuclear cells decreased in number and macrophages became arranged in large clusters.
The expression of α-SM actin in fibroblastic cells of the granulation tissue started from the 4th day after pump implantation
and progressed up to the 7th day. Double immunofluorescence staining showed macrophage clusters in relation to α-SM actinrich
fibroblastic cells. Electron microscopic examination confirmed that the fibroblasts containing α-SM actinpositive stress fibers
were found initially in close proximity to clustered macrophages. The delivery of plateletderived growth factor (PDGF) and
tumor necrosis factor-α (TNF-α) by the osmotic minipump induced an accumulation of macrophages, but in a much smaller number
compared with those seen after GM-CSF application; these macrophages were never assembled in clusters and, furthermore, TNF-α
and PDGF did not stimulate α-SM actin expression in fibroblastic cells. Our results suggest that after GM-CSF administration,
the cluster-like accumulation of macrophages plays an important role in stimulating α-SM actin expression in myofibroblasts.
Our results may be relevant to the understanding of the processes leading to granulation tissue formation in this and other
experimental models. 相似文献
18.
Christophe M. R. LeMoine Stephen C. Lougheed Christopher D. Moyes 《Journal of molecular evolution》2010,70(5):492-505
In mammals, the peroxisome proliferator activated receptor (PPAR)γ coactivator-1α (PGC-1α) is a central regulator of mitochondrial
gene expression, acting in concert with nuclear respiratory factor-1 (NRF-1) and the PPARs. Its role as a “master regulator”
of oxidative capacity is clear in mammals, but its role in other vertebrates is ambiguous. In lower vertebrates, although
PGC-1α seems to play a role in coordinating the PPARα axis as in mammals, it does not appear to be involved in NRF-1 regulation
of mitochondrial content. To evaluate the evolutionary patterns of this coactivator in fish and mammals, we investigated the
evolutionary trajectories of PGC-1α homologs in representative vertebrate lineages. A phylogeny of the PGC-1 paralogs suggested
that the family diversified through repeated genome duplication events early in vertebrate evolution. Bayesian and maximum
likelihood phylogenetic reconstructions of PGC-1α in representative vertebrate species revealed divergent evolutionary dynamics
across the different functional domains of the protein. Specifically, PGC-1α exhibited strong conservation of the activation/PPAR
interaction domain across vertebrates, whereas the NRF-1 and MEF2c interaction domains experienced accelerated rates of evolution
in actinopterygian (fish lineages) compared to sarcopterygians (tetrapod lineages). Furthermore, analysis of the amino acid
sequence of these variable domains revealed successive serine- and glutamine-rich insertions within the teleost lineages,
with important ramifications for PGC-1α function in these lineages. Collectively, these results suggest modular evolution
of the PGC-1α protein in vertebrates that could allow for lineage-specific divergences in the coactivating capabilities of
this regulator. 相似文献
19.
Shan-chuan Zhong Xue Luo Xing-shu Chen Qi-yan Cai Jing Liu Xing-hua Chen Zhong-xiang Yao 《Cellular and molecular neurobiology》2010,30(3):469-482
Alpha-synuclein (α-SYN) is one of the major components of intracellular fibrillary aggregates in the brains of a subset of
neurodegenerative disorders. Although α-SYN expression has been found in developing mouse brain, a detailed distribution during
mouse-embryonic development has not been made. Here we describe the expression pattern of α-SYN during the development of
mice from E9.5 to P0 by immunohistochemistry (IHC). As a result, α-SYN was detected as early as E9.5. During the embryonic
stages, α-SYN was dynamically expressed in several regions of the brain. In the neocortex, expression was detected in the
marginal zone (MZ) in the early stages and was later condensed in the MZ and in the subplate (SP); in the cerebellum, expression
was initially detected in the deep cerebellar nuclei (DCN) and was later condensed in the Purkinje cells. These spatio-temporal
expression patterns matched the neuronal migratory pathways and the formation of the synapse connections. Additionally, α-SYN
was detected in the sensory systems, including the nasal mucosa, the optic cup, the sensory ganglia, and their dominating
nerve fibers. Furthermore, the nuclear location of α-SYN protein was found in developing neurons in the early stages, and
later it was mostly found in the non-nuclear compartments. This finding was further confirmed by Western blot analysis. These
results suggest that α-SYN may be involved not only in the migration of neurons and in the synaptogenesis of the central nervous
system (CNS) but also in the establishment of the sensory systems. The nuclear location of α-SYN may hint at an important
function in these events. 相似文献
20.
The interphase nucleus and nuclear envelope can acquire a myriad of shapes in normal or pathological cell states. There exist
a wide variety of indentations and invaginations, of protrusions and evaginations. It has been difficult to classify and name
all of these nuclear shapes and, consequently, a barrier to understanding the biochemical and biophysical causes. This review
focuses upon one type of nuclear envelope shape change, named “nuclear envelope-limited chromatin sheets” (ELCS), which appears
to involve exaggerated nuclear envelope growth, carrying with it one or more layers of ∼30 nm diameter heterochromatin. A
hypothesis on the formation of ELCS is proposed, relating higher order heterochromatin structure in an interphase nucleus,
nuclear envelope growth, and nuclear envelope-heterochromatin interactions. 相似文献