Relevant bibliographies by topics / Hox genes

Academic literature on the topic 'Hox genes'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Hox genes.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Hox genes"

1

Lin, Hou, Chen Zhijuan, Xu Mingyu, Lin Shengguo, and Wang Lu. "Hox genes and study of Hox genes in crustacean." Chinese Journal of Oceanology and Limnology 22, no. 4 (December 2004): 392–98. http://dx.doi.org/10.1007/bf02843634.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Snape, Alison. "Regulating Hox genes." Trends in Genetics 15, no. 1 (January 1999): 14. http://dx.doi.org/10.1016/s0168-9525(98)01676-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Nazarali, A., Y. Kim, and M. Nirenberg. "Hox-1.11 and Hox-4.9 homeobox genes." Proceedings of the National Academy of Sciences 89, no. 7 (April 1, 1992): 2883–87. http://dx.doi.org/10.1073/pnas.89.7.2883.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Hrycaj, Steven M., and Deneen M. Wellik. "Hox genes and evolution." F1000Research 5 (May 10, 2016): 859. http://dx.doi.org/10.12688/f1000research.7663.1.

Full text
Abstract:
Hox proteins are a deeply conserved group of transcription factors originally defined for their critical roles in governing segmental identity along the antero-posterior (AP) axis in Drosophila. Over the last 30 years, numerous data generated in evolutionarily diverse taxa have clearly shown that changes in the expression patterns of these genes are closely associated with the regionalization of the AP axis, suggesting that Hox genes have played a critical role in the evolution of novel body plans within Bilateria. Despite this deep functional conservation and the importance of these genes in AP patterning, key questions remain regarding many aspects of Hox biology. In this commentary, we highlight recent reports that have provided novel insight into the origins of the mammalian Hox cluster, the role of Hox genes in the generation of a limbless body plan, and a novel putative mechanism in which Hox genes may encode specificity along the AP axis. Although the data discussed here offer a fresh perspective, it is clear that there is still much to learn about Hox biology and the roles it has played in the evolution of the Bilaterian body plan.
APA, Harvard, Vancouver, ISO, and other styles
5

Marshall, Heather, Alastair Morrison, Michèle Studer, Heike Pöpperl, and Robb Krumlauf. "Retinoids and Hox genes." FASEB Journal 10, no. 9 (July 1996): 969–78. http://dx.doi.org/10.1096/fasebj.10.9.8801179.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Vitiello, Danielle, Pinar Kodaman, and Hugh Taylor. "HOX Genes in Implantation." Seminars in Reproductive Medicine 25, no. 6 (November 2007): 431–36. http://dx.doi.org/10.1055/s-2007-991040.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ruddle, F. H., J. L. Bartels, K. L. Bentley, C. Kappen, M. T. Murtha, and J. W. Pendleton. "Evolution of Hox Genes." Annual Review of Genetics 28, no. 1 (December 1994): 423–42. http://dx.doi.org/10.1146/annurev.ge.28.120194.002231.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Botti, Gerardo, Clemente Cillo, Rossella De Cecio, Maria Gabriella Malzone, and Monica Cantile. "Paralogous HOX13 Genes in Human Cancers." Cancers 11, no. 5 (May 20, 2019): 699. http://dx.doi.org/10.3390/cancers11050699.

Full text
Abstract:
Hox genes (HOX in humans), an evolutionary preserved gene family, are key determinants of embryonic development and cell memory gene program. Hox genes are organized in four clusters on four chromosomal loci aligned in 13 paralogous groups based on sequence homology (Hox gene network). During development Hox genes are transcribed, according to the rule of “spatio-temporal collinearity”, with early regulators of anterior body regions located at the 3’ end of each Hox cluster and the later regulators of posterior body regions placed at the distal 5’ end. The onset of 3’ Hox gene activation is determined by Wingless-type MMTV integration site family (Wnt) signaling, whereas 5’ Hox activation is due to paralogous group 13 genes, which act as posterior-inhibitors of more anterior Hox proteins (posterior prevalence). Deregulation of HOX genes is associated with developmental abnormalities and different human diseases. Paralogous HOX13 genes (HOX A13, HOX B13, HOX C13 and HOX D13) also play a relevant role in tumor development and progression. In this review, we will discuss the role of paralogous HOX13 genes regarding their regulatory mechanisms during carcinogenesis and tumor progression and their use as biomarkers for cancer diagnosis and treatment.
APA, Harvard, Vancouver, ISO, and other styles
9

Bogue, C. W., I. Gross, H. Vasavada, D. W. Dynia, C. M. Wilson, and H. C. Jacobs. "Identification of Hox genes in newborn lung and effects of gestational age and retinoic acid on their expression." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 4 (April 1, 1994): L448—L454. http://dx.doi.org/10.1152/ajplung.1994.266.4.l448.

Full text
Abstract:
Hox genes are sequence-specific DNA transcription factors, which are important in embryonic development and are expressed in a number of fetal tissues, including the lung. Additionally, retinoic acid (RA) has been shown to modulate Hox gene expression in a number of cell types. The specific aims of this study were to 1) identify those Hox genes expressed in newborn mouse lung using reverse transcription-polymerase chain reaction (RT-PCR), 2) study the ontogeny of Hox gene expression in fetal mouse and rat lung by Northern analysis using cDNAs for mouse Hox genes, and 3) study the effects of RA on whole lung Hox mRNA levels in cultured fetal rat lung explants. Our data show that 16 different homeobox genes are expressed in newborn mouse lung. This includes seven Hox genes not previously identified in lung, as well as the divergent homeobox gene Hex. Steady-state mRNA levels of Hox A5 (Hox 1.3), B5 (Hox 2.1), B6 (Hox 2.2), and B8 (Hox 2.4) decrease with advancing gestational age in mouse lungs (E14 to adult). Similarly, Hox A5, B5, and B6 follow the same decreasing pattern of expression with advancing gestational age in rat lungs (E15 to adult). RA treatment of E17 rat lung explants in culture resulted in a significant dose- and time-dependent increase in Hox A5, B5, and B6 mRNA levels. The highest mRNA levels were seen in explants treated with 1 x 10(-5) M RA for 4-16 h. We conclude that there are many homeobox genes expressed in developing rodent lung and that their mRNA levels are affected by both gestational age and RA.
APA, Harvard, Vancouver, ISO, and other styles
10

Strathdee, Gordon R., Tessa L. Holyoake, Alyson Sim, Anton Parker, David G. Oscier, Junia V. Melo, Stefan Meyer, et al. "HOX Genes - Candidate Tumor Suppressor Genes in Adult and Childhood Leukemia." Blood 110, no. 11 (November 16, 2007): 2641. http://dx.doi.org/10.1182/blood.v110.11.2641.2641.

Full text
Abstract:
Abstract The role of the HOX gene family in leukemia development has been extensively studied. However, these studies have focused almost exclusively on the potential oncogenic role of HOX gene family members. In contrast to the oncogenic function often attributed to HOX genes, our studies have identified several HOX gene family members as candidate tumor suppressor genes and shown that inactivation of HOX genes, particularly HOXA4, is associated with poor prognosis. We have used multiple quantitative methylation assays to search for epigenetic inactivation of HOX genes in adult and childhood leukemia. In both adult myeloid and lymphoid leukemia two members of the HOXA cluster (HOXA4 and A5) were found to be frequently inactivated by promoter hypermethylation (26–64% of cases were hypermethylated). In contrast, a further 12 HOXA, B and C cluster genes were found to be essentially devoid of hypermethylation (except HOXA6 in CLL, where 34% of samples exhibited hypermethylation). HOXA4 and HOXA5 were also frequently inactivated in childhood ALL and AML (39–79% of samples). However, in contrast to the adult leukemias, all but one of the additional HOX genes analyzed were also found to be targets for hypermethylation in both ALL and AML (4–26% of samples), suggesting that HOX genes are differentially regulated in childhood versus adult leukemia. Hypermethylation of HOX genes (HOXA4, HOXA5 and HOXA6) was associated with loss of expression of the corresponding gene. Expression analysis also suggests that interaction between different HOX genes may be crucial. In normal karyotype AML samples, those expressing of high levels of HOXA9, but not those with low HOXA9 expression, were associated with invariable HOXA4 hypermethylation (p=0.01). Interestingly HOXA4 hypermethylation also correlates with poor prognosis in all types of leukemia tested. Hypermethylation of HOXA4 correlates with progression to blast crisis (p=0.007) and poor response to imatinib in CML (p=0.04), with cytogenetic status in AML (33%, 72% and 100% in good, intermediate and poor prognostic groups respectively, p=0.0004) and with IgVh mutational status (p=0.003) and poor survival in CLL (median survival 159 versus 199 months in hypermethylated and non hypermethylated patients, respectively). Furthermore transfection of a HOXA4 expressing construct into a CML blast crisis cell line results in re-expression of markers of myeloid differentiation, suggesting that loss of HOXA4 is functionally relevant in leukemic cells. These results indicate that aberrant epigenetic regulation of HOXA4, and indeed other frequently inactivated HOX genes such as HOXA5 and HOXA6, may play a key role in the development of multiple types of leukemia. Thus co-ordinated up and down regulation of expression of HOX gene family members may be crucial in the leukemogenic process.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Hox genes"

1

Averof, Michalis. "HOM/Hox genes of a crustacean : evolutionary implications." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319512.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Zhou, Bo. "Structural studies of geminin-hox and smad-hox complexes /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BICH%202007%20ZHOU.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Svingen, Terje, and n/a. "Hox Transcription Factors: Their Involvement in Human Cancer Cells and In Vitro Functional Specificity." Griffith University. School of Biomolecular and Biomedical Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20050830.135356.

Full text
Abstract:
Hox genes are regulatory genes encoding small proteins containing a highly conserved 61-amino acid motif, the homeodomain, that enables Hox proteins to bind to DNA at specifically recognised binding sites and transcriptionally activate their target genes. In mammalian species there are 39 Hox genes and they are structural and functional homologs of the Drosophila homeotic complex (Horn-C). During embryogenesis and early development the Hox genes are expressed in a spatiotemporal fashion, where they operate as master transcriptional regulators. Hox genes are further expressed in fully differentiated adult cells, potentially in a tissue-specific manner involving maintenance of the normal phenotype. In selected oncogenic transformations, dysregulated Hox gene expression has been observed, indicating an involvement of these transcriptional regulators in carcinogenesis and metastasis. Utilising quantitative real-time PCR assays, these studies investigated the expression patterns of 20 Hox genes and two wellcharacterised Hox cofactors (Pbx and Meis) in malignant and non-malignant human breast and skin cancer cells. Dysregulated Hox expression was observed for all malignancies tested, of which some misexpressed Hox genes seemed random, whereas other Hox transcripts showed altered levels potentially corresponding with the invasive capacity of the cells. Also, the Hox cofactors Pbx and Meis showed no marked changes in expression levels from the non-malignant to the malignant phenotypes, indicating that it is dysregulated Hox gene expression rather than dysregulated gene expression of Hox cofactors that potentially commit the cell to redifferentiate and undergo oncogenic transformation. Although the Hox proteins are known to be key transcriptional regulators of development, the mechanisms by which they gain their in vivo functional specificity is still largely unknown. They all show strikingly similar transcriptional specificity in vitro, yet show unique specificity in their in vivo environment. This paradox has been the subject of intense scrutiny, however very few direct Hox target genes have been identified, making it a difficult task to decipher the exact manner in which Hox proteins exert their functional potential. Therefore, the studies presented herein were aimed at identifying further Hox target genes in the human system. Utilising differential display approaches, several potential downstream target genes were isolated. Substantiated with real-time PCR assays, one of these potential targets was selected as a likely direct Hox gene target, and as such subjected to further studies. By the combination of bioinformatic analyses, transfection protocols and luciferase assays, a gene encoding the SR-related protein SRrpl3O was shown to be trans-activated in vitro by HOXD4 via a putative Hox binding element within its promoter region. This is the first reported link between Hox transcription factors and the SR and SR-related family of pre-mRNA splicing proteins, offering a new and exciting insight into the complex nature of Hox functional specificity. Finally, this thesis also puts forward new ideas regarding how the Hox proteins gain their transcriptional and functional specificity. Utilising bioinformatic tools in conjunction with performing an extensive review of the disparate catalogue of Hox-related research reports, work herein offers the first comprehensive analysis of the mammalian Hox gene targets in relation to their promoter structures, as well as with respect to the expanded Hox DNA-binding elements. This work reports that identified Hox targets generally contain TATA-less core promoters, many of which have several GC-box elements. The Hox binding elements show no apparent preference regarding their location relative to the transcription start site (TSS), as they are found both upstream and downstream of the TSS, as well as being located close to proximal core promoter elements for some genes and at more distant positions in other gene promoters. Finally, the core Hox binding element TAAT/ATTA contains only part of the necessary recognition sequence involved in Hox-DNA binding, and the notion that flanking base pairs dictate trans-regulatory potential is further explored with the hypothesis that the immediate 3' base pair dictates an activator/repressor-switch of the Hox trans-regulatory effect.
APA, Harvard, Vancouver, ISO, and other styles
4

Svingen, Terje. "Hox Transcription Factors: Their Involvement in Human Cancer Cells and In Vitro Functional Specificity." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365774.

Full text
Abstract:
Hox genes are regulatory genes encoding small proteins containing a highly conserved 61-amino acid motif, the homeodomain, that enables Hox proteins to bind to DNA at specifically recognised binding sites and transcriptionally activate their target genes. In mammalian species there are 39 Hox genes and they are structural and functional homologs of the Drosophila homeotic complex (Horn-C). During embryogenesis and early development the Hox genes are expressed in a spatiotemporal fashion, where they operate as master transcriptional regulators. Hox genes are further expressed in fully differentiated adult cells, potentially in a tissue-specific manner involving maintenance of the normal phenotype. In selected oncogenic transformations, dysregulated Hox gene expression has been observed, indicating an involvement of these transcriptional regulators in carcinogenesis and metastasis. Utilising quantitative real-time PCR assays, these studies investigated the expression patterns of 20 Hox genes and two wellcharacterised Hox cofactors (Pbx and Meis) in malignant and non-malignant human breast and skin cancer cells. Dysregulated Hox expression was observed for all malignancies tested, of which some misexpressed Hox genes seemed random, whereas other Hox transcripts showed altered levels potentially corresponding with the invasive capacity of the cells. Also, the Hox cofactors Pbx and Meis showed no marked changes in expression levels from the non-malignant to the malignant phenotypes, indicating that it is dysregulated Hox gene expression rather than dysregulated gene expression of Hox cofactors that potentially commit the cell to redifferentiate and undergo oncogenic transformation. Although the Hox proteins are known to be key transcriptional regulators of development, the mechanisms by which they gain their in vivo functional specificity is still largely unknown. They all show strikingly similar transcriptional specificity in vitro, yet show unique specificity in their in vivo environment. This paradox has been the subject of intense scrutiny, however very few direct Hox target genes have been identified, making it a difficult task to decipher the exact manner in which Hox proteins exert their functional potential. Therefore, the studies presented herein were aimed at identifying further Hox target genes in the human system. Utilising differential display approaches, several potential downstream target genes were isolated. Substantiated with real-time PCR assays, one of these potential targets was selected as a likely direct Hox gene target, and as such subjected to further studies. By the combination of bioinformatic analyses, transfection protocols and luciferase assays, a gene encoding the SR-related protein SRrpl3O was shown to be trans-activated in vitro by HOXD4 via a putative Hox binding element within its promoter region. This is the first reported link between Hox transcription factors and the SR and SR-related family of pre-mRNA splicing proteins, offering a new and exciting insight into the complex nature of Hox functional specificity. Finally, this thesis also puts forward new ideas regarding how the Hox proteins gain their transcriptional and functional specificity. Utilising bioinformatic tools in conjunction with performing an extensive review of the disparate catalogue of Hox-related research reports, work herein offers the first comprehensive analysis of the mammalian Hox gene targets in relation to their promoter structures, as well as with respect to the expanded Hox DNA-binding elements. This work reports that identified Hox targets generally contain TATA-less core promoters, many of which have several GC-box elements. The Hox binding elements show no apparent preference regarding their location relative to the transcription start site (TSS), as they are found both upstream and downstream of the TSS, as well as being located close to proximal core promoter elements for some genes and at more distant positions in other gene promoters. Finally, the core Hox binding element TAAT/ATTA contains only part of the necessary recognition sequence involved in Hox-DNA binding, and the notion that flanking base pairs dictate trans-regulatory potential is further explored with the hypothesis that the immediate 3' base pair dictates an activator/repressor-switch of the Hox trans-regulatory effect.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Full Text
APA, Harvard, Vancouver, ISO, and other styles
5

Ackema, K. B. "Hox genes and mesenchymal stem cells." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Smith, Margaret Louise. "An analysis of Hox genes in Myriapods." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624853.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Plaça, Jessica Rodrigues. "Avaliação do perfil genômico dos genes da família HOX em tumores a partir de dados de bancos públicos." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-17042018-161612/.

Full text
Abstract:
A família de genes HOX compreende um conjunto de fatores de transcrição altamente conservados evolutivamente. Em mamíferos, os genes HOX se subdividem em 4 clusters: HOXA, HOXB, HOXC e HOXD, atuando no desenvolvimento embrionário com a regulação de processos biológicos como proliferação, diferenciação, migração, angiogênese e apoptose que são reativados durante a carcinogênese. Estudos recentes apontam que os genes HOX podem exercer papel relevante na formação de diversos tumores sólidos, todavia ainda não foi possível caracterizar sistematicamente a expressão dos genes HOX em tumores bem como determinar seus alvos em tumores. Desta forma, o objetivo geral deste trabalho consistiu na caracterização in silico do modelo de atuação genes HOX na carcinogênese. Para cumprir este objetivo foi identificado o perfil diferencial dos genes HOX entre amostras normais e tumorais. Alvos de genes HOX foram identificados e, quando diferencialmente expressos, foram associados com os genes HOX, independentemente dos índices de metilação e CNA. Por fim, as associações finais entre os genes HOX e seus alvos foram enriquecidas com os bancos de dados KEGG e GO. Identificou-se diferentes assinaturas de expressão de genes HOX em diferentes tumores, associadas com o eixo ântero-posterior do corpo humano, bem como os folhetos embrionários originários aos tecidos tumorais, compatível com o padrão de expressão no desenvolvimento embrionário. Um número considerável de genes HOX atuam preferencialmente via enhancers na regulação de seus alvos. Como exemplo, os genes HOXB7 e HOXC11, que funcionam como moduladores anti tumorais. Finalmente, o estudo mostra que diante do número crescente de dados genômicos públicos, é possível viabilizar projetos de grande valor científico.
The HOX gene family comprises a set of evolutionarily highly conserved transcription factors. In mammals, HOX genes are subdivided into four clusters: HOXA, HOXB, HOXC and HOXD, acting on the embryonic development with regulation of biological processes such as proliferation, differentiation, migration, angiogenesis and apoptosis that are reactivated during carcinogenesis. Recent studies indicate that HOX genes may play a relevant role in the formation of several solid tumors, but it has not been possible to systematically characterize the expression of HOX genes in tumors as well as to determine their targets in tumors. Thus, the general aim of this project was to characterize the in vivo model of HOX genes in carcinogenesis. To accomplish this goal the differential profile of HOX genes was identified between normal and tumor samples. HOX gene targets were identified and, when differentially expressed, were associated with HOX genes regardless of methylation and CNA indices. Finally, the final associations between the HOX genes and their targets were enriched with the KEGG and GO databases. Different signatures of HOX gene expression were identified in different tumors, associated with the anteroposterior axis of the human body, as well as the embryonic leaflets originating from the tumor tissues, compatible with the expression pattern in the embryonic development. A considerable number of HOX genes preferentially act via enhancers in the regulation of their targets. As an example, the HOXB7 and HOXC11 genes, which function as pro-tumor modulators. Finally, the study shows that in view of the growing number of public genomic data, it is possible to make feasible projects of great scientific value.
APA, Harvard, Vancouver, ISO, and other styles
8

Pearce, Jonathan J. H. "Murine chromobox genes and the maintenance of Hox gene expression patterns." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282013.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Lincoln, Joy. "Developmental studies of the murine homeobox gene, Hoxa-9." Thesis, Durham University, 2002. http://etheses.dur.ac.uk/4145/.

Full text
Abstract:
Cell patterning during embryogenesis is essential for establishing the identity of the developing body plan. Hox genes are fundamental regulators of tissue organisation along the anterior-posterior body axis of the developing embryo. These homeodomain-containing proteins act as transcription factors during normal development. The function of the homeodomain is to bind sequence-specific DNAmotifs which allows either activation or repression of downstream effector genes, which consequently results in the control of tissue-specific determination and differentiation. Aberrant expression of such Hox genes, including Hoxa-9 can result in homeotic transformations leading to phenotypic malformations and oncogenesis. However the normal function of Hoxa-9 is poorly understood. This study explored the potential role for Hoxa-9 in normal development and differentiation. An in situ hybridisation approach was taken to define the expression of Hoxa-9 in the developing mouse. Hoxa-9 was found to expressed in a temporarily and spatially regulated manner, in particular being detected in the developing cardiac atria, ventricles and cardiac vessels during E9.5-E12 stages of development. The expression of this homeotic gene during in vitro differentiation of embryonic stem cells into cardiomyocytes and haematopoietic cells demonstrated a profile that correlated with the emergence of these cell types. The functioning relationship between Hoxa-9 expression and lineage commitment was Airther explored using over-expression in embryonic stem cells. A potential role for Hoxa-9 in normal development is discussed.
APA, Harvard, Vancouver, ISO, and other styles
10

Caronia, Giuliana. "A 147L substitution in the HOXD13 homeodomain causes a novel human limb malformation by producing a selective loss of function." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275109.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Hox genes"

1

service), ScienceDirect (Online, ed. Hox genes. Amsterdam: Elsevier, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Deutsch, Jean S., ed. Hox Genes. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6673-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Graba, Yacine, and René Rezsohazy, eds. Hox Genes. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1242-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Graba, Yacine. Hox genes: Methods and protocols. New York: Humana Press, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hox genes: Studies from the 20th to the 21st century. New York: Springer Science+Business Media, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Geada, AntÆnio Moreno Colao. Analysis of the two most 3' genes of the Hox-c cluster. Manchester: University of Manchester, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

J, Greenspan Ralph, and Kendler Kenneth S. 1950-, eds. How genes influence behavior. Oxford: Oxford University Press, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Flint, Jonathan. How genes influence behavior. New York, NY: Oxford University Press, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Coming to life: How genes drive development. San Diego, CA: Kales Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

United States. Congress. Office of Technology Assessment., ed. Mapping our genes: Genome projects--how big, how fast? Baltimore: Johns Hopkins University Press, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Hox genes"

1

Kulp, Jennifer L., Hakan Cakmak, and Hugh S. Taylor. "HOX Genes and Endometriosis." In Endometriosis, 184–89. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781444398519.ch18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Omori, Akihito, and Naoki Irie. "Hox Genes in Echinoderms." In Hox Modules in Evolution and Development, 141–60. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003057215-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wollesen, Tim, and Andreas Wanninger. "Hox Genes in Mollusca." In Hox Modules in Evolution and Development, 161–76. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003057215-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Allmen, Gretchen Von, Iiham Hogga, Anne Spierer, François Karch, Welcome Bender, Henrik Gyurkovics, and E. B. Lewis. "Splits in Fruitfly Hox Gene Complexes." In Genes, Development, and Cancer, 403–5. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6345-9_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

von Allmen, Gretchen, Iiham Hogga, Anne Spierer, François Karch, Welcome Bender, Henrik Gyurkovics, and E. B. Lewis. "Splits in Fruitfly Hox Gene Complexes." In Genes, Development and Cancer, 377–79. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8981-9_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Castelli-Gair Hombría, J., C. Sánchez-Higueras, and E. Sánchez-Herrero. "Control of Organogenesis by Hox Genes." In Organogenetic Gene Networks, 319–73. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42767-6_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Fibi, M., M. Kessel, and P. Gruss. "Murine Hox Genes — A Multigene Family." In Genetics of Immunological Diseases, 82–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-50059-6_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Dick, M. H. "Hox genes and annelid-arthropod relationships." In Arthropod Relationships, 35–41. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4904-4_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Gąsiorowski, Ludwik, José M. Martín-Durán, and Andreas Hejnol. "The Evolution of Hox Genes in Spiralia." In Hox Modules in Evolution and Development, 177–94. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003057215-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Reichert, Heinrich, and Bruno Bello. "Hox Genes and Brain Development in Drosophila." In Advances in Experimental Medicine and Biology, 145–53. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6673-5_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Hox genes"

1

Coletta, Ricardo D., Carolina C. Bitu, Manoela Pereira, Marcio A. Lopes, and Edgard Graner. "Abstract 2028: HOX genes in oral cancer: Expression profile and functional characterization." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2028.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Osmond, Brian, Caroline O. Facey, Lynn M. Opdenaker, and Bruce M. Boman. "Abstract 3089: Study of HOX genes in the stem cell origin of CRC." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-3089.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

"Expression and role of hox genes in the regeneration of internal organs in the sea cucumber Eupentacta fraudatrix." In SYSTEMS BIOLOGY AND BIOINFORMATICS. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/sbb-2019-12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bhatlekar, Seema, Kirk Czymmek, Vignesh Viswanathan, Greg Gonye, and Bruce Boman. "Abstract LB-102: Role of HOX genes in regulation of stem cell populations in normal and malignant colon tissue." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-102.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wang, Rui, Guoqing Wang, Joumana Ahmed, and Ronald G. Crystal. "Positional Identity Of Branching-Associated Hox Genes Is Maintained By Human Airway Epithelial Progenitor Cells Obtained From Different Sites In The Tracheobronchial Tree." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1241.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Luo, Li Z., Ewa Krawczyk, Anbarasu Lourdusamy, Lisa C. Storer, Lingling Xian, Kenneth J. Cohen, Richard Schlegel, Richard Grundy, and Linda Resar. "Abstract LB-224: A novel model of pediatric spinal ependymoma using conditionally reprogrammed cells from a primary tumor demonstrates aberrant expression ofHMGA, HOX, MYCand other Wnt target genes." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-224.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Neitz, Jay, Maureen Neitz, and Gerald H. Jacobs. "More than three cone types in normal color vision?" In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/oam.1990.fm6.

Full text
Abstract:
Normal human color vision is usually thought to be based on only three spectrally different cone types. However, two facts suggest the possibility that some color-normal males could have more than three cone pigment types: (1) Most people with normal color vision have more than two photopigment genes on each X-chromosome and (2) there appear to be genetically specified variations in spectral positions of the normal middle-wavelength-sensitive (MWS) and long-wavelength-sensitive (LWS) pigments. For example, a male might have one gene encoding an LWS pigment and two genes encoding slightly different MWS pigments. If all three different X-encoded genes were expressed in different cones, then this person would have four spectrally different cone types. How firm is the assumption that more than two of the X-encoded pigment genes can be expressed? Both analysis of the statistics of photopigment gene number among different color vision phenotypes and analysis of the arrangement of pigment genes on the X-chromosome yield insight into this aspect of photopigment gene expression. These analyses suggest that individuals with multiple pigment genes on the X-chromosome may express more than two of those genes.
APA, Harvard, Vancouver, ISO, and other styles
8

Zaccaron, Alex. "Impact of genomic structural variations on virulence of the tomato pathogen Cladosporium fulvum." In IS-MPMI Congress. IS-MPMI, 2023. http://dx.doi.org/10.1094/ismpmi-2023-1.

Full text
Abstract:
Cladosporium fulvum causes tomato leaf mold and has been extensively used in the past as a model species to study plant-microbe interactions. Although the first chromosome-scale reference genome of the fungus was released in 2022, still little is known about how its genome architecture and structural variations (SVs) thereof impact its virulence. In this study, we used PacBio HiFi to sequence the genomes of four additional C. fulvum isolates and further assembled them at chromosome level. Comparative genome analyses revealed high chromosomal synteny among the five isolates, and a set of 13 core and two dispensable chromosomes, one of which carries pseudogenized copies of effector genes and likely emerged by duplication of subtelomeric regions of core chromosome. Between 14906 and 14993 genes were predicted in each C. fulvum genome with an estimated completeness of >99%. A pangenome analysis of the five isolates revealed a low number of 331 accessory genes, indicating high conservation of gene content among isolates of the fungus. An analysis of SVs showed no enriched of effectors or of other pathogenicity-related genes in these regions. However, SVs in subtelomeric regions affected virulence by prompting the loss of effector genes residing in them, as we have found is the case for the Avr9 effector gene of C. fulvum. Collectively, these results provide new insights of how genomic SVs can contribute to virulence of fungal pathogens.
APA, Harvard, Vancouver, ISO, and other styles
9

Salazar Moscoso, Marcela, Silvia Joly Ruiz Castellanos, Guillem Anglada Escudé, and Laia Ribas Cabezas. "Hypergravity induces changes in physiology, gene expression and epigenetics in zebrafish." In Symposium on Space Educational Activities (SSAE). Universitat Politècnica de Catalunya, 2022. http://dx.doi.org/10.5821/conference-9788419184405.044.

Full text
Abstract:
All living organisms that inhabit Earth have evolved under a common value of gravity, which amounts to an acceleration of 9.81 m/s2 at mean sea level. Changes on it could cause important alterations that affect vital biological functions. The crescent interest in spatial exploration has opened the question of how exactly these changes in gravity would affect Earth life forms on space environments. This work is the result of a collaborative co-supervision of a master thesis between experts in the area of space sciences and biology, and it can serve as a case study for training experts in such interdisciplinary environments. In particular, we focus on the effect of gravity as a pressure factor in the development of zebrafish (Danio rerio) in the larval stage as a model organism using up-to-date (genomic and epigenetic) techniques. Given the high cost of any experiment in true low gravity (which would require a space launch), we performed an initial experiment in hypergravity to develop the methodologies and identify good (epi)genetic markers of the effect of gravity in our model organism. Previous studies in zebrafish have shown how alteration in gravity effects the development and the gene expression of important regulatory genes. For this study, we firstly customized a small laboratory scale centrifuge to study changes in fish physiology together with changes at molecular levels. We exposed zebrafish larvae from 0 to 6 days post fertilization to the simulated hypergravity (SHG) (100 rpm  3g). After 6 days of hypergravity exposition the larvae showed changes in their swimming and flotation patterns, and presented corporal alterations. Then, we assessed gene expression of genes implicated in important biological processes, (e.g., epigenetics), and an upregulation were observed when compared to the control. Taken together, these preliminary findings show how gravity alterations could affect some basic biological responses, and illustrate the potential of developing new science cases to be developed by students at postgraduate level (MSc and beyond) in a multidisciplinary environment
APA, Harvard, Vancouver, ISO, and other styles
10

Angelotti, Austin, Rachel Cole, Amy Webb, Maciej Pietrzak, and Martha Belury. "Diet-induced Gene Expression Changes of Cachectic Muscle, Adipose, and Liver." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/gvbe2596.

Full text
Abstract:
Cancer cachexia is a systemic disease characterized by muscle and adipose loss that cannot be reversed by increasing caloric intake. Our previous research has shown insulin resistance precedes cancer cachexia in the C26 mouse model of cachexia, and a diet high in linoleic acid, the essential omega-6 polyunsaturated fatty acid, attenuates the C26-induced insulin resistance. Therefore, to better understand how dietary linoleic acid is improving insulin sensitivity, we characterized gene expression changes in three major tissues responsible for controlling insulin sensitivity: skeletal muscle, adipose, and liver. To do this male CD2F1 (Charles River, MA) were randomized to semi-purified diet (24% fat by weight) containing fat prominently from lard, or containing fat prominently from safflower oil (a linoleic acid-rich oil). One week after diet randomization, mice were inoculated with colon-26 (C26) adenocarcinoma cells (1.0E6 cells). 13 days after inoculation mice were euthanized and gastrocnemius skeletal muscle, epididymal white adipose tissue, and liver tissue were collected for total transcriptome analysis using poly-A enriched next generation RNA-sequencing. Differentially expressed genes were selected based on p-values < 0.05. There were no detectable differences in body weight or food intake between the two diets in mice with C26 tumors. Between the two diets 12 genes were differentially expressed in the muscle, while 57 genes were differentially expressed in the liver, and 314 genes were differentially expressed in adipose. A linoleic acid enriched diet had little effect on the skeletal muscle transcriptome but induced larger transcriptome changes in liver and adipose. This could suggest dietary linoleic acid increases insulin sensitivity through affecting metabolism in adipose and liver, rather than skeletal muscle. Determining these diet-induced transcriptome changes allows us to better target tissue-specific molecular mechanisms of linoleic acid in future research.
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Hox genes"

1

none,. Mapping our genes: The genome projects: How big, how fast. Office of Scientific and Technical Information (OSTI), April 1988. http://dx.doi.org/10.2172/5113312.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Michelmore, Richard, Eviatar Nevo, Abraham Korol, and Tzion Fahima. Genetic Diversity at Resistance Gene Clusters in Wild Populations of Lactuca. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7573075.bard.

Full text
Abstract:
Genetic resistance is often the least expensive, most effective, and ecologically-sound method of disease control. It is becoming apparent that plant genomes contain large numbers of disease resistance genes. However, the numbers of different resistance specificities within a genepool and the genetic mechanisms generating diversity are poorly understood. Our objectives were to characterize diversity in clusters of resistance genes in wild progenitors of cultivated lettuce in Israel and California in comparison to diversity within cultivated lettuce, and to determine the extent of gene flow, recombination, and genetic instability in generating variation within clusters of resistance genes. Genetic diversity of resistance genes was analyzed in wild and cultivated germplasm using molecular markers derived from lettuce resistance gene sequences of the NBS-LRR type that mapped to the major cluster if resistance genes in lettuce (Sicard et al. 1999). Three molecular markers, one microsatellite marker and two SCAR markers that amplified LRR- encoding regions, were developed from sequences of resistance gene homologs at the Dm3 cluster (RGC2s) in lettuce. Variation for these markers was assessed in germplasm including 74 genotypes of cultivated lettuce, L. saliva and 71 accessions of the three wild Lactuca spp., L. serriola, L. saligna and L. virosa that represent the major species in the sexually accessible genepool for lettuce. Diversity was also studied within and between natural populations of L. serriola from Israel and California. Large numbers of haplotypes were detected indicating the presence of numerous resistance genes in wild species. We documented a variety of genetic events occurring at clusters of resistance genes for the second objective (Sicard et al., 1999; Woo el al., in prep; Kuang et al., in prepb). The diversity of resistance genes in haplotypes provided evidence for gene duplication and unequal crossing over during the evolution of this cluster of resistance genes. Comparison of nine resistance genes in cv. Diana identified 22 gene conversion and five intergenic recombinations. We cloned and sequenced a 700 bp region from the middle of RGC2 genes from six genotypes, two each from L. saliva, L. serriola, and L. saligna . We have identified over 60 unique RGC2 sequences. Phylogenetic analysis surprisingly demonstrated much greater similarity between than within genotypes. This led to the realization that resistance genes are evolving much slower than had previously been assumed and to a new model as to how resistance genes are evolving (Michelmore and Meyers, 1998). The genetic structure of L. serriola was studied using 319 AFLP markers (Kuang et al., in prepa). Forty-one populations from Turkey, Armenia, Israel, and California as well as seven European countries were examined. AFLP marker data showed that the Turkish and Armenian populations were the most polymorphic populations and the European populations were the least. The Davis, CA population, a recent post-Columbian colonization, showed medium genetic diversity and was genetically close to the Turkish populations. Our results suggest that Turkey - Armenia may be the center of origin and diversity of L. serriola and may therefore have the greatest diversity of resistance genes. Our characterization of the diversity of resistance genes and the genetic mechanisms generating it will allow informed exploration, in situ and ex situ conservation, and utilization of germplasm resources for disease control. The results of this project provide the basis for our future research work, which will lead to a detailed understanding of the evolution of resistance genes in plants.
APA, Harvard, Vancouver, ISO, and other styles
3

Viputheshwar Sitaraman, Viputheshwar Sitaraman. How to edit any gene. Experiment, July 2014. http://dx.doi.org/10.18258/2852.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Heifetz, Yael, and Michael Bender. Success and failure in insect fertilization and reproduction - the role of the female accessory glands. United States Department of Agriculture, December 2006. http://dx.doi.org/10.32747/2006.7695586.bard.

Full text
Abstract:
The research problem. Understanding of insect reproduction has been critical to the design of insect pest control strategies including disruptions of mate-finding, courtship and sperm transfer by male insects. It is well known that males transfer proteins to females during mating that profoundly affect female reproductive physiology, but little is known about the molecular basis of female mating response and no attempts have yet been made to interfere with female post-mating responses that directly bear on the efficacy of fertilization. The female reproductive tract provides a crucial environment for the events of fertilization yet thus far those events and the role of the female tract in influencing them are poorly understood. For this project, we have chosen to focus on the lower reproductive tract because it is the site of two processes critical to reproduction: sperm management (storage, maintenance, and release from storage) and fertilization. E,fforts during this project period centered on the elucidation of mating responses in the female lower reproductive tract The central goals of this project were: 1. To identify mating-responsive genes in the female lower reproductive tract using DNA microarray technology. 2. In parallel, to identify mating-responsive genes in these tissues using proteomic assays (2D gels and LC-MS/MS techniques). 3. To integrate proteomic and genomic analyses of reproductive tract gene expression to identify significant genes for functional analysis. Our main achievements were: 1. Identification of mating-responsive genes in the female lower reproductive tract. We identified 539 mating-responsive genes using genomic and proteomic approaches. This analysis revealed a shift from gene silencing to gene activation soon after mating and a peak in differential gene expression at 6 hours post-mating. In addition, comparison of the two datasets revealed an expression pattern consistent with the model that important reproductive proteins are pre-programmed for synthesis prior to mating. This work was published in Mack et al. (2006). Validation experiments using real-time PCR techniques suggest that microarray assays provide a conservativestimate of the true transcriptional activity in reproductive tissues. 2.lntegration of proteomics and genomics data sets. We compared the expression profiles from DNA microarray data with the proteins identified in our proteomic experiments. Although comparing the two data sets poses analyical challenges, it provides a more complete view of gene expression as well as insights into how specific genes may be regulated. This work was published in Mack et al. (2006). 3. Development of primary reproductive tract cell cultures. We developed primary cell cultures of dispersed reproductive tract cell types and determined conditions for organ culture of the entire reproductive tract. This work will allow us to rapidly screen mating-responsive genes for a variety of reproductive-tract specifi c functions. Scientific and agricultural significance. Together, these studies have defined the genetic response to mating in a part of the female reproductive tract that is critical for successful fertllization and have identified alarge set of mating-responsive genes. This work is the first to combine both genomic and proteomic approaches in determining female mating response in these tissues and has provided important insights into insect reproductive behavior.
APA, Harvard, Vancouver, ISO, and other styles
5

Rodriguez, Russell J., and Stanley Freeman. Gene Expression Patterns in Plants Colonized with Pathogenic and Non-pathogenic Gene Disruption Mutants of Colletotrichum. United States Department of Agriculture, February 2009. http://dx.doi.org/10.32747/2009.7592112.bard.

Full text
Abstract:
Fungal plant pathogens are responsible for extensive annual crop and revenue losses throughout the world. To better understand why fungi cause diseases, we performed gene-disruption mutagenesis on several pathogenic Colletotrichum species and demonstrated that pathogenic isolates can be converted to symbionts expressing non-pathogenic lifestyles. One group of nonpathogenic mutants confer disease protection against pathogenic species of Col!etotrichum, Fusarium and Phytophthora; drought tolerance; and growth enhancement to host plants. These mutants have been defined as mutualists and disease resistance correlates to a decrease in the time required for hosts to activate defense systems when exposed to virulent fungi. A second group of non-pathogenic mutants did not confer disease resistance and were classified as commensals. In addition, we have demonstrated that wildtype pathogenic Colletotrichum species can express non-pathogenic lifestyles, including mutualism, on plants they colonize asymptomatically. We have been using wildtype and isogenic gene disruption mutants to characterize gene expression patterns in plants colonized with a pathogen, mutualist or commensal. The US group is contrasting genes expressed during colonization by mutuahstic and commensal mutants of C. magna and a pathogenic wildtype C. coccodes on tomato. The Israeli group is characterizing genes expressed during asymptomatic colonization of tomato by wildtype C. acutatum and a non-pathogenic mutant.To accomplish this we have been utilizing suppressive subtraction hybridization, microarray and sequencing strategies. The expected contribution of this research to agriculture in the US and Israel is: 1) understanding how pathogens colonize certain hosts asymptomatic ally will shed light on the ecology of plant pathogens which has been described as a fundamental deficiency in plant pathology; 2) identifying genes involved in symbiotically conferred disease resistance will help explain why and how pathogens cause disease, and may identify new candidate targets for developing genetically modified disease resistant crop plants.
APA, Harvard, Vancouver, ISO, and other styles
6

Li, Li, Joseph Burger, Nurit Katzir, Yaakov Tadmor, Ari Schaffer, and Zhangjun Fei. Characterization of the Or regulatory network in melon for carotenoid biofortification in food crops. United States Department of Agriculture, April 2015. http://dx.doi.org/10.32747/2015.7594408.bard.

Full text
Abstract:
The general goals of the BARD research grant US-4423-11 are to understand how Or regulates carotenoid accumulation and to reveal novel strategies for breeding agricultural crops with enhanced β-carotene level. The original objectives are: 1) to identify the genes and proteins in the Or regulatory network in melon; 2) to genetically and molecularly characterize the candidate genes; and 3) to define genetic and functional allelic variation of these genes in a representative germplasm collection of the C. melo species. Or was found by the US group to causes provitamin A accumulation in chromoplasts in cauliflower. Preliminary genetic study from the Israeli group revealed that the melon Or gene (CmOr) completely co-segregated with fruit flesh color in a segregating mapping population and in a wide melon germplasm collection, which set the stage for the funded research. Major conclusions and achievements include: 1). CmOris proved to be the gene that controls melon fruit flesh color and represents the previously described gflocus in melon. 2). Genetic and molecular analyses of CmOridentify and confirm a single SNP that is responsible for the orange and non-orange phenotypes in melon fruit. 3). Alteration of the evolutionarily conserved arginine in an OR protein to both histidine or alanine greatly enhances its ability to promote carotenoid accumulation. 4). OR promotes massive carotenoid accumulation due to its dual functions in regulating both chromoplast biogenesis and carotenoid biosynthesis. 5). A bulk segregant transcriptome (BSRseq) analysis identifies a list of genes associated with the CmOrregulatory network. 6). BSRseq is proved to be an effective approach for gene discovery. 7). Screening of an EMS mutation library identifies a low β mutant, which contains low level of carotenoids due to a mutation in CmOrto produce a truncated form of OR protein. 8). low β exhibits lower germination rate and slow growth under salt stress condition. 9). Postharvest storage of fruit enhances carotenoid accumulation, which is associated with chromoplast development. Our research uncovers the molecular mechanisms underlying the Or-regulated high level of carotenoid accumulation via regulating carotenoidbiosynthetic capacity and storage sink strength. The findings provide mechanistic insights into how carotenoid accumulation is controlled in plants. Our research also provides general and reliable molecular markers for melon-breeding programs to select orange varieties, and offers effective genetic tools for pro-vitamin A enrichment in other important crops via the rapidly developed genome editing technology. The newly discovered low β mutant could lead to a better understanding of the Or gene function and its association with stress response, which may explain the high conservation of the Or gene among various plant species.
APA, Harvard, Vancouver, ISO, and other styles
7

Levin, Ilan, John W. Scott, Moshe Lapidot, and Moshe Reuveni. Fine mapping, functional analysis and pyramiding of genes controlling begomovirus resistance in tomato. United States Department of Agriculture, November 2014. http://dx.doi.org/10.32747/2014.7594406.bard.

Full text
Abstract:
Abstract. Tomato yellow leaf curl virus (TYLCV), a monopartitebegomovirus, is one of the most devastating viruses of cultivated tomatoes and poses increasing threat to tomato production worldwide. Because all accessions of the cultivated tomato are susceptible to these viruses, wild tomato species have become a valuable resource of resistance genes. QTL controlling resistance to TYLCV and other begomoviruses (Ty loci) were introgressed from several wild tomato species and mapped to the tomato genome. Additionally, a non-isogenic F₁diallel study demonstrated that several of these resistance sources may interact with each other, and in some cases generate hybrid plants displaying lower symptoms and higher fruit yield compared to their parental lines, while their respective resistance genes are not necessarily allelic. This suggests that pyramiding genes originating from different resistance sources can be effective in obtaining lines and cultivars which are highly resistant to begomoviruses. Molecular tools needed to test this hypothesis have been developed by our labs and can thus significantly improve our understanding of the mechanisms of begomovirus resistance and how to efficiently exploit them to develop wider and more durable resistance. Five non-allelic Ty loci with relatively major effects have been mapped to the tomato genome using molecular DNA markers, thereby establishing tools for efficient marker assisted selection, pyramiding of multiple genes, and map based gene cloning: Ty-1, Ty-2, Ty-3, Ty-4, and ty-5. This research focused on Ty-3 and Ty-4 due to their broad range of resistance to different begomoviruses, including ToMoV, and on ty-5 due to its exceptionally high level of resistance to TYLCV and other begomoviruses. Our aims were: (1) clone Ty-3, and fine map Ty-4 and Ty-5 genes, (2)introgress each gene into two backgroundsand develop semi isogenic lines harboring all possible combinations of the three genes while minimizing linkage-drag, (3) test the resulting lines, and F₁ hybrids made with them, for symptom severity and yield components, and (4) identify and functionally characterize candidate genes that map to chromosomal segments which harbor the resistance loci. During the course of this research we have: (1) found that the allelic Ty-1 and Ty-3 represent two alternative alleles of the gene coding DFDGD-RDRP; (2) found that ty-5is highly likely encoded by the messenger RNA surveillance factor PELOTA (validation is at progress with positive results); (3) continued the map-based cloning of Ty-4; (4) generated all possible gene combinations among Ty-1, Ty-3 and ty-5, including their F₁ counterparts, and tested them for TYLCV and ToMoV resistance; (5) found that the symptomless line TY172, carrying ty-5, also carries a novel allele of Ty-1 (termed Ty-1ⱽ). The main scientific and agricultural implications of this research are as follows: (1) We have developed recombination free DNA markers that will substantially facilitate the introgression of Ty-1, Ty-3 and ty-5 as well as their combinations; (2) We have identified the genes controlling TYLCV resistance at the Ty-1/Ty-3 and ty-5 loci, thus enabling an in-depth analyses of the mechanisms that facilitate begomovirus resistance; (3) Pyramiding of Ty resistance loci is highly effective in providing significantly higher TYLCV resistance.
APA, Harvard, Vancouver, ISO, and other styles
8

Case, Anne, I.-Fen Lin, and Sara McLanahan. How Hungry is the Selfish Gene? Cambridge, MA: National Bureau of Economic Research, October 1999. http://dx.doi.org/10.3386/w7401.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ling Hsiao, Ray, Yu Wei Lin, and Chiang Yun Chen. Supplementary Information of Innovative Observation of a 266-nm Laser Inhibiting Egg Laying in Caenorhabditis elegans. Science Repository, July 2022. http://dx.doi.org/10.31487/j.acr.2022.02.04.sup.

Full text
Abstract:
Infrared laser as a heat source could induce gene expression by activating heat promoter genes in Caenorhabditis elegans, as previously reported. In this study, we innovatively used a 266-nm laser to irradiate C. elegans for only one second and observed a significant inhibition of the overall number of eggs laid (P < 0.0001) and the first day egg laying (P=0.005). This is the first study to establish how light with a wavelength of 266-nm can influence a life activity such as laying eggs in C. elegans.
APA, Harvard, Vancouver, ISO, and other styles
10

Pawlowski, Wojtek P., and Avraham A. Levy. What shapes the crossover landscape in maize and wheat and how can we modify it. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600025.bard.

Full text
Abstract:
Meiotic recombination is a process in which homologous chromosomes engage in the exchange of DNA segments, creating gametes with new genetic makeup and progeny with new traits. The genetic diversity generated in this way is the main engine of crop improvement in sexually reproducing plants. Understanding regulation of this process, particularly the regulation of the rate and location of recombination events, and devising ways of modifying them, was the major motivation of this project. The project was carried out in maize and wheat, two leading crops, in which any advance in the breeder’s toolbox can have a huge impact on food production. Preliminary work done in the USA and Israeli labs had established a strong basis to address these questions. The USA lab pioneered the ability to map sites where recombination is initiated via the induction of double-strand breaks in chromosomal DNA. It has a long experience in cytological analysis of meiosis. The Israeli lab has expertise in high resolution mapping of crossover sites and has done pioneering work on the importance of epigenetic modifications for crossover distribution. It has identified genes that limit the rates of recombination. Our working hypothesis was that an integrative analysis of double-strand breaks, crossovers, and epigenetic data will increase our understanding of how meiotic recombination is regulated and will enhance our ability to manipulate it. The specific objectives of the project were: To analyze the connection between double-strand breaks, crossover, and epigenetic marks in maize and wheat. Protocols developed for double-strand breaks mapping in maize were applied to wheat. A detailed analysis of existing and new data in maize was conducted to map crossovers at high resolution and search for DNA sequence motifs underlying crossover hotspots. Epigenetic modifications along maize chromosomes were analyzed as well. Finally, a computational analysis tested various hypotheses on the importance of chromatin structure and specific epigenetic modifications in determining the locations of double-strand breaks and crossovers along chromosomes. Transient knockdowns of meiotic genes that suppress homologous recombination were carried out in wheat using Virus-Induced Gene Silencing. The target genes were orthologs of FANCM, DDM1, MET1, RECQ4, and XRCC2.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Hox genes' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography