• Molecules and Cells
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• 제26권3호
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• pp.217-227
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• 2008

Heterochromatin protein 1 (HP1) was first described in Drosophila melanogaster as a heterochromatin associated protein with dose-dependent effect on gene silencing. The HP1 family is evolutionarily highly conserved and there are multiple members within the same species. The multi-functionality of HP1 reflects its ability to interact with diverse nuclear proteins, ranging from histones and transcriptional co-repressors to cohesion and DNA replication factors. As its name suggests, HP1 is well-known as a silencing protein found at pericentromeres and telomeres. In contrast to previous views that heterochromatin is transcriptionally inactive; noncoding RNAs transcribed from heterochromatic DNA repeats regulates the assembly and function of heterochromatin ranging from fission yeast to animals. Moreover, more recent progress has shed light on the paradoxical properties of HP1 in the nucleus and has revealed, unexpectedly, its existence in the euchromatin. Therefore, HP1 proteins might participate in both transcription repression in heterochromatin and euchromatin.

• BMB Reports
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• 제55권3호
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• pp.111-112
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• 2022

We visualized the distribution of heterochromatin in a single nucleus using plasmonic nanoparticle-conjugated H3K9me3 and H3K27me3 antibodies. Due to distance-dependent plasmonic coupling effects between nanoprobes, their scattering spectra shift to longer wavelengths as the distance between heterochromatin histone markers reduced during oncogene-induced senescence (OIS). These observations were supported by simulating scattering profiles based on considerations of particle numbers, interparticle distances, and the spatial arrangements of plasmonic nanoprobes. Using this plasmon-based colourimetric imaging, we estimated changes in distances between H3K9me3 and H3K27me3 during the formation of senescence-associated heterochromatin foci in OIS cells. We anticipate that the devised analytical technique combined with high-spatial imaging and spectral simulation will eventually lead to a new means of diagnosing and monitoring disease progression and cellular senescence.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2001년도 한국생물과학협회 학술발표대회
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• pp.237.3-238
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• 2001

No Abstract, See Full Text

• 한국가금학회지
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• 제17권4호
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• pp.275-280
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• 1990

Constitutive heterochromatin의 염색체 다형현상에 대해 사람을 비롯하여 돼지, 생쥐, 말, 닭 등에서 보고된 바 있다. 본 연구에서는 일본산메추리의 C－band 다형체 뿐만 아니라 염색체의 형태적 다형체를 발견하여 이의 다형현상을 밝혔다. 일반적인 염색체 분석방법 및 C－banding 방법으로서 밝힌 3가지 염색체 다형체는 4번 염색체 ＋/－ 동형체, ＋/－ 이형체 및 －/－ 동형체이다. 이와 같은 다형체들은 무작위 집단 내에서 일반적이고 지속적으로 나타나며 Mendel 법칙에 따른 유전양상을 보인다. 따라서 본 연구에서 밝힌 염색체 다형체들은 여러 세포유전학적 연구에 표식인자(chromosome marker)로서 유용하게 이용되어질 수 있을 것으로 생각된다.

• Journal of Genetic Medicine
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• 제14권2호
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• pp.62-66
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• 2017

Interchromosomal insertion of Y chromosome heterochromatin in an autosome was identified in a fetus and a family. A fetal karyotype was analyzed as 46,XX,dup(7)(?q22q21.1) in a referred amniocentesis at 16 weeks of gestation for advanced maternal age. In the familial karyotype analyses for identification of der(7), the mother, the first daughter and the maternal grandmother showed the same der(7) as the fetus's. CBG-banding was positive at 7q22 region of der(7) that indicated inserted material was originated from heterochromatin. The origin of heterochromatic insertion region in der(7) of the fetus and the mother was found in Yq12 region by fluorescent in situ hybridization with a DYZ1 probe. In the specific analysis of Y chromosomal heterochromatic region of ins(7;Y) of the mother, 15 sequence tagged sites from Yp11.3 region including SRY to Yq11.223 region was not detected. Final karyotypes of the mother, the first daughter and the maternal grandmother were reported as 46,XX,der(7)ins(7;Y)(q21.3;q12q12). All female carriers of ins(7;Y) in the family showed normal phenotype and the mother and the maternal grandmother were fertile. A healthy girl was born at term. We report a rare case of familial interchromosomal insertion of Y chromosome heterochromatin detected only in female family members with normal phenotype that was diagnosed prenatally.

• Journal of Plant Biology
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• 제18권3호
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• pp.92-100
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• 1975

The present study demonstrates karyotype based on H-patterns of A.fistulosum and A. ascalonicum using Giemsa technique. The results obtained in this study are summarized as follows: I). Karyotypic analysis of A. fistulosum is 6VII＋$JII^t＋JII$ and that of A. ascalonicum collected from a local farm in the suberbs of Taegu city clearly heterozygous as $13V＋J_1^t＋J_2＋i. ii$). The heterochromatin of both species is generally located distally in both arms of chromosomes and each chromosome type possesses some variations on H-patterns. iii). The percentage of heterochromatin to total chromosome length in cell is about 14.6% in A. fistulosum, 12.8% in A. ascalonicum. The number of bands is revealed about 38 in A. fistulosum and 33 in A. ascalonicum. Also in the amounts of chromocenters per nucleus, the former is somewhat more than the latter.

• Biomolecules & Therapeutics
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• 제22권4호
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• pp.308-313
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• 2014

Activator protein-1 (AP-1) is an inducible transcription factor that contributes to the generation of chronic inflammation in response to oxidative and electrophilic stress. Previous studies have demonstrated that the PI3K/Akt1 pathway plays an important role in the transcriptional regulation of AP-1 expression. Although the histone post-translational modifications (PTMs) are assumed to affect the AP-1 transcriptional regulation by the PI3K/Akt pathway, the detailed mechanisms are completely unknown. In the present study, we show that heterochromatin 1 gamma ($HP1{\gamma}$) plays a negative role in TPA-induced c-Jun and c-Fos expression. We show that TPA-induced Akt1 directly phosphorylates $HP1{\gamma}$, abrogates its suppressive function and increases the interaction between histone H3 and 14-3-$3{\varepsilon}$. Collectively, these our data illustrate that the activation of PI3K/Akt pathway may play a permissive role in the recruitment of histone readers or other coactivators on the chromatin, thereby affecting the degree of AP-1 transcription.

• 한국안광학회지
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• 제1권1호
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• pp.15-22
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• 1996

본 연구는 망막조직의 미세구조를 전자현미경을 이용하여, 생쥐(ICR)에 대한 Laser 조사의 영향을 조사하였다. 그 결과는 다음과 같다. l. 정상군에서 대개의 망막층은 여러 특수한 세포들과 신경섬유로 구성된 복잡한 구조를 가지고 있었다. 2. Laser 조사의 기간이 길어질수록, 망막의 각 세포의 층과 구조는 일정한 형태를 나타내지 못했다. 시세포 visual cell들은 심하게 이형염색질체 heterochromatin이며, 세포질은 종대되며, 핵의 모양은 불규칙적이며,일부의 세포질은 소실되었다. 망막층의 핵과 신경섬유는 매우 불규칙적이며, 소포의 형성, 각 세포간 경계의 불명확함이 있었다. 색소상피세포 pigment epithelail cell들은 정상모양이 아니며, 세포질에는 큰 공포 형성이 있으며, 핵의 응축과 불규칙한 모양 등이 있었다.

• BMB Reports
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• 제41권7호
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• pp.523-528
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• 2008

BMI-1026 is a synthetic aminopyrimidine compound that targets cyclin dependent kinases (cdks) and was initially designed as a potential anticancer drug. Even though it has been well documented that BMI-1026 is a potent cdk inhibitor, little is known about the cellular effects of this compound. In this study, we examined the effects of BMI-1026 treatment on inducing premature senescence and then evaluated the biochemical features of BMI-1026-induced premature senescence. From these experiments we determined that BMI-1026 treatment produced several biochemical features of premature senescence and also stimulated expression of mitogen activated protein kinase (MAPK) family proteins. BMI-1026 treatment caused nuclear translocation of activated Erk1/2 and the formation of senescence associated heterochromatin foci in 5 days. The heterochromatin foci formation was perturbed by inhibition of Erk1/2 activation.

• Genomics & Informatics
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• 제11권4호
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• pp.164-173
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• 2013

Genomic instability, which occurs through both genetic mechanisms (underlying inheritable phenotypic variations caused by DNA sequence-dependent alterations, such as mutation, deletion, insertion, inversion, translocation, and chromosomal aneuploidy) and epigenomic aberrations (underlying inheritable phenotypic variations caused by DNA sequence-independent alterations caused by a change of chromatin structure, such as DNA methylation and histone modifications), is known to promote tumorigenesis and tumor progression. Mechanisms involve both genomic instability and epigenomic aberrations that lose or gain the function of genes that impinge on tumor suppression/prevention or oncogenesis. Growing evidence points to an epigenome-wide disruption that involves large-scale DNA hypomethylation but specific hyper-methylation of tumor suppressor genes, large blocks of aberrant histone modifications, and abnormal miRNA expression profile. Emerging molecular details regarding the modulation of these epigenetic events in cancer are used to illustrate the alterations of epigenetic molecules, and their consequent malfunctions could contribute to cancer biology. More recently, intriguing evidence supporting that genetic and epigenetic mechanisms are not separate events in cancer has been emerging; they intertwine and take advantage of each other during tumorigenesis. In addition, we discuss the collusion between epigenetics and genetics mediated by heterochromatin protein 1, a major component of heterochromatin, in order to maintain genome integrity.