Keith Maggert

Interests

Research

Chromatin, Gene regulation, Epigenetics, Repeat gene stability, Genetics, Transposable elements / transposons / retrotransposable elements / retrotransposons, Satellite DNA, Chromosome biology and cytogenetics

Courses

Scholarly Contributions

Journals/Publications

• Bughio, F., & Maggert, K. (2021). Live Analysis of Position Effect Variegation (PEV) in Drosophila Reveals Different Modes of Action for HP1 and Su(var)3-9. Proceedings of the National Academy of Sciences.
• Kindelay, S., & Maggert, K. (2021). Ribosomal DNA Copy Number Variation – origins, implications, effects. Seminars in Cell and Development Biology on Ribosome Homeostasis.
• Lebeau, L., Maggert, K. A., Valori, V., Tus, K., Maggert, K. A., Lebeau, L., Laukaitis, C. M., & Harris, D. T. (2020). Human rDNA copy number is unstable in metastatic breast cancers.. Epigenetics, 15(1-2), 85-106. doi:10.1080/15592294.2019.1649930
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  Chromatin-mediated silencing, including the formation of heterochromatin, silent chromosome territories, and repressed gene promoters, acts to stabilize patterns of gene regulation and the physical structure of the genome. Reduction of chromatin-mediated silencing can result in genome rearrangements, particularly at intrinsically unstable regions of the genome such as transposons, satellite repeats, and repetitive gene clusters including the rRNA gene clusters (rDNA). It is thus expected that mutational or environmental conditions that compromise heterochromatin function might cause genome instability, and diseases associated with decreased epigenetic stability might exhibit genome changes as part of their aetiology. We find the support of this hypothesis in invasive ductal breast carcinoma, in which reduced epigenetic silencing has been previously described, by using a facile method to quantify rDNA copy number in biopsied breast tumours and pair-matched healthy tissue. We found that rDNA and satellite DNA sequences had significant copy number variation - both losses and gains of copies - compared to healthy tissue, arguing that these genome rearrangements are common in developing breast cancer. Thus, any proposed aetiology onset or progression of breast cancer should consider alterations to the epigenome, but must also accommodate concomitant changes to genome sequence at heterochromatic loci.
• Ji, J., Tang, X., Hu, W., Maggert, K., & Rong, Y. (2019). Pol32 mediates nuclear localization of DNA polymerase δ and prevents chromosomal fragile site formation in Drosophila development. PLoS-Genetics.
• Maggert, K. A. (2019). Stress: An evolutionary mutagen. Proceedings of the National Academy of Sciences of the United States of America, 116(36), 17616-17618.
• Maggert, K., Valori, V., Laukaitis, C. M., Lebeau, L., Harris, D. T., & Tus, K. (2019). Human rDNA Copy Number Is Unstable in Developing Breast Cancers. Epigenetics.
• Aldrich, J. C., & Maggert, K. A. (2015). Transgenerational inheritance of diet-induced genome rearrangements in Drosophila. PLoS genetics, 11(4), e1005148.
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  Ribosomal RNA gene (rDNA) copy number variation modulates heterochromatin formation and influences the expression of a large fraction of the Drosophila genome. This discovery, along with the link between rDNA, aging, and disease, high-lights the importance of understanding how natural rDNA copy number variation arises. Pursuing the relationship between rDNA expression and stability, we have discovered that increased dietary yeast concentration, emulating periods of dietary excess during life, results in somatic rDNA instability and copy number reduction. Modulation of Insulin/TOR signaling produces similar results, indicating a role for known nutrient sensing signaling pathways in this process. Furthermore, adults fed elevated dietary yeast concentrations produce offspring with fewer rDNA copies demonstrating that these effects also occur in the germline, and are transgenerationally heritable. This finding explains one source of natural rDNA copy number variation revealing a clear long-term consequence of diet.
• Bughio, F., & Maggert, K. A. (2019). The peculiar genetics of the ribosomal DNA blurs the boundaries of transgenerational epigenetic inheritance. Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology.
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  Our goal is to draw a line-hypothetical in its totality but experimentally supported at each individual step-connecting the ribosomal DNA and the phenomenon of transgenerational epigenetic inheritance of induced phenotypes. The reasonableness of this hypothesis is offset by its implication, that many (or most) (or all) of the cases of induced-and-inherited phenotypes that are seen to persist for generations are instead unmapped induced polymorphisms in the ribosomal DNA, and thus are the consequence of the peculiar and enduringly fascinating genetics of the highly transcribed repeat DNA structure at that locus.
• Deans, C., & Maggert, K. A. (2015). What do you mean, "epigenetic"?. Genetics, 199(4), 887-96.
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  Interest in the field of epigenetics has increased rapidly over the last decade, with the term becoming more identifiable in biomedical research, scientific fields outside of the molecular sciences, such as ecology and physiology, and even mainstream culture. It has become increasingly clear, however, that different investigators ascribe different definitions to the term. Some employ epigenetics to explain changes in gene expression, others use it to refer to transgenerational effects and/or inherited expression states. This disagreement on a clear definition has made communication difficult, synthesis of epigenetic research across fields nearly impossible, and has in many ways biased methodologies and interpretations. This article discusses the history behind the multitude of definitions that have been employed since the conception of epigenetics, analyzes the components of these definitions, and offers solutions for clarifying the field and mitigating the problems that have arisen due to these definitional ambiguities.
• Aldrich, J. C., & Maggert, K. A. (2014). Simple quantitative PCR approach to reveal naturally occurring and mutation-induced repetitive sequence variation on the Drosophila Y chromosome. PloS one, 9(10), e109906.
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  Heterochromatin is a significant component of the human genome and the genomes of most model organisms. Although heterochromatin is thought to be largely non-coding, it is clear that it plays an important role in chromosome structure and gene regulation. Despite a growing awareness of its functional significance, the repetitive sequences underlying some heterochromatin remain relatively uncharacterized. We have developed a real-time quantitative PCR-based method for quantifying simple repetitive satellite sequences and have used this technique to characterize the heterochromatic Y chromosome of Drosophila melanogaster. In this report, we validate the approach, identify previously unknown satellite sequence copy number polymorphisms in Y chromosomes from different geographic sources, and show that a defect in heterochromatin formation can induce similar copy number polymorphisms in a laboratory strain. These findings provide a simple method to investigate the dynamic nature of repetitive sequences and characterize conditions which might give rise to long-lasting alterations in DNA sequence.
• Maggert, K. A. (2014). Reduced rDNA copy number does not affect "competitive" chromosome pairing in XYY males of Drosophila melanogaster. G3 (Bethesda, Md.), 4(3), 497-507.
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  The ribosomal DNA (rDNA) arrays are causal agents in X-Y chromosome pairing in meiosis I of Drosophila males. Despite broad variation in X-linked and Y-linked rDNA copy number, polymorphisms in regulatory/spacer sequences between rRNA genes, and variance in copy number of interrupting R1 and R2 retrotransposable elements, there is little evidence that different rDNA arrays affect pairing efficacy. I investigated whether induced rDNA copy number polymorphisms affect chromosome pairing in a "competitive" situation in which complex pairing configurations were possible using males with XYY constitution. Using a common normal X chromosome, one of two different full-length Y chromosomes, and a third chromosome from a series of otherwise-isogenic rDNA deletions, I detected no differences in X-Y or Y-Y pairing or chromosome segregation frequencies that could not be attributed to random variation alone. This work was performed in the context of an undergraduate teaching program at Texas A&M University, and I discuss the pedagogical utility of this and other such experiments.
• Maggert, K. A. (2012). Genetics: polymorphisms, epigenetics, and something in between. Genetics research international, 2012, 867951.
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  At its broadest sense, to say that a phenotype is epigenetic suggests that it occurs without changes in DNA sequence, yet is heritable through cell division and occasionally from one organismal generation to the next. Since gene regulatory changes are oftentimes in response to environmental stimuli and may be retained in descendent cells, there is a growing expectation that one's experiences may have consequence for subsequent generations and thus impact evolution by decoupling a selectable phenotype from its underlying heritable genotype. But the risk of this overbroad use of "epigenetic" is a conflation of genuine cases of heritable non-sequence genetic information with trivial modes of gene regulation. A look at the term "epigenetic" and some problems with its increasing prevalence argues for a more reserved and precise set of defining characteristics. Additionally, questions arising about how we define the "sequence independence" aspect of epigenetic inheritance suggest a form of genome evolution resulting from induced polymorphisms at repeated loci (e.g., the rDNA or heterochromatin).
• Guerrero, P. A., & Maggert, K. A. (2011). The CCCTC-binding factor (CTCF) of Drosophila contributes to the regulation of the ribosomal DNA and nucleolar stability. PloS one, 6(1), e16401.
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  In the repeat array of ribosomal DNA (rDNA), only about half of the genes are actively transcribed while the others are silenced. In arthropods, transposable elements interrupt a subset of genes, often inactivating transcription of those genes. Little is known about the establishment or separation of juxtaposed active and inactive chromatin domains, or preferential inactivation of transposable element interrupted genes, despite identity in promoter sequences. CTCF is a sequence-specific DNA binding protein which is thought to act as a transcriptional repressor, block enhancer-promoter communication, and delimit juxtaposed domains of active and inactive chromatin; one or more of these activities might contribute to the regulation of this repeated gene cluster. In support of this hypothesis, we show that the Drosophila nucleolus contains CTCF, which is bound to transposable element sequences within the rDNA. Reduction in CTCF gene activity results in nucleolar fragmentation and reduced rDNA silencing, as does disruption of poly-ADP-ribosylation thought to be necessary for CTCF nucleolar localization. Our data establish a role for CTCF as a component necessary for proper control of transposable element-laden rDNA transcription and nucleolar stability.
• Paredes, S., Branco, A. T., Hartl, D. L., Maggert, K. A., & Lemos, B. (2011). Ribosomal DNA deletions modulate genome-wide gene expression: "rDNA-sensitive" genes and natural variation. PLoS genetics, 7(4), e1001376.
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  The ribosomal rDNA gene array is an epigenetically-regulated repeated gene locus. While rDNA copy number varies widely between and within species, the functional consequences of subtle copy number polymorphisms have been largely unknown. Deletions in the Drosophila Y-linked rDNA modifies heterochromatin-induced position effect variegation (PEV), but it has been unknown if the euchromatic component of the genome is affected by rDNA copy number. Polymorphisms of naturally occurring Y chromosomes affect both euchromatin and heterochromatin, although the elements responsible for these effects are unknown. Here we show that copy number of the Y-linked rDNA array is a source of genome-wide variation in gene expression. Induced deletions in the rDNA affect the expression of hundreds to thousands of euchromatic genes throughout the genome of males and females. Although the affected genes are not physically clustered, we observed functional enrichments for genes whose protein products are located in the mitochondria and are involved in electron transport. The affected genes significantly overlap with genes affected by natural polymorphisms on Y chromosomes, suggesting that polymorphic rDNA copy number is an important determinant of gene expression diversity in natural populations. Altogether, our results indicate that subtle changes to rDNA copy number between individuals may contribute to biologically relevant phenotypic variation.
• Alfonso-Parra, C., & Maggert, K. A. (2010). Drosophila SAF-B links the nuclear matrix, chromosomes, and transcriptional activity. PloS one, 5(4), e10248.
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  Induction of gene expression is correlated with alterations in nuclear organization, including proximity to other active genes, to the nuclear cortex, and to cytologically distinct domains of the nucleus. Chromosomes are tethered to the insoluble nuclear scaffold/matrix through interaction with Scaffold/Matrix Attachment Region (SAR/MAR) binding proteins. Identification and characterization of proteins involved in establishing or maintaining chromosome-scaffold interactions is necessary to understand how the nucleus is organized and how dynamic changes in attachment are correlated with alterations in gene expression. We identified and characterized one such scaffold attachment factor, a Drosophila homolog of mammalian SAF-B. The large nuclei and chromosomes of Drosophila have allowed us to show that SAF-B inhabits distinct subnuclear compartments, forms weblike continua in nuclei of salivary glands, and interacts with discrete chromosomal loci in interphase nuclei. These interactions appear mediated either by DNA-protein interactions, or through RNA-protein interactions that can be altered during changes in gene expression programs. Extraction of soluble nuclear proteins and DNA leaves SAF-B intact, showing that this scaffold/matrix-attachment protein is a durable component of the nuclear matrix. Together, we have shown that SAF-B links the nuclear scaffold, chromosomes, and transcriptional activity.
• Paredes, S., & Maggert, K. A. (2009). Expression of I-CreI endonuclease generates deletions within the rDNA of Drosophila. Genetics, 181(4), 1661-71.
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  The rDNA arrays in Drosophila contain the cis-acting nucleolus organizer regions responsible for forming the nucleolus and the genes for the 28S, 18S, and 5.8S/2S RNA components of the ribosomes and so serve a central role in protein synthesis. Mutations or alterations that affect the nucleolus organizer region have pleiotropic effects on genome regulation and development and may play a role in genomewide phenomena such as aging and cancer. We demonstrate a method to create an allelic series of graded deletions in the Drosophila Y-linked rDNA of otherwise isogenic chromosomes, quantify the size of the deletions using real-time PCR, and monitor magnification of the rDNA arrays as their functions are restored. We use this series to define the thresholds of Y-linked rDNA required for sufficient protein translation, as well as establish the rate of Y-linked rDNA magnification in Drosophila. Finally, we show that I-CreI expression can revert rDNA deletion phenotypes, suggesting that double-strand breaks are sufficient to induce rDNA magnification.
• Paredes, S., & Maggert, K. A. (2009). Ribosomal DNA contributes to global chromatin regulation. Proceedings of the National Academy of Sciences of the United States of America, 106(42), 17829-34.
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  The 35S ribosomal RNA genes (rDNA) are organized as repeated arrays in many organisms. Epigenetic regulation of transcription of the rRNA results in only a subset of copies being transcribed, making rDNA an important model for understanding epigenetic chromatin modification. We have created an allelic series of deletions within the rDNA array of the Drosophila Y chromosome that affect nucleolus size and morphology, but do not limit steady-state rRNA concentrations. These rDNA deletions result in reduced heterochromatin-induced gene silencing elsewhere in the genome, and the extent of the rDNA deletion correlates with the loss of silencing. Consistent with this, chromosomes isolated from strains mutated in genes required for proper heterochromatin formation have very small rDNA arrays, reinforcing the connection between heterochromatin and the rDNA. In wild-type cells, which undergo spontaneous natural rDNA loss, we observed the same correlation between loss of rDNA and loss of heterochromatin-induced silencing, showing that the volatility of rDNA arrays may epigenetically influence gene expression through normal development and differentiation. We propose that the rDNA contributes to a balance between heterochromatin and euchromatin in the nucleus, and alterations in rDNA--induced or natural--affect this balance.
• Maggert, K. A., Gong, W. J., & Golic, K. G. (2008). Methods for homologous recombination in Drosophila. Methods in molecular biology (Clifton, N.J.), 420, 155-74.
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  We present detailed protocols for two methods of gene targeting in Drosophila. The first, ends-out targeting, is identical in concept to gene replacement techniques used routinely in mammalian and yeast cells. In Drosophila, the targeted gene is replaced by the marker gene white + (although options exist to generate unmarked targeted alleles). This approach is simple in both the molecular cloning and the genetic manipulations. Ends-out will likely serve most investigators' purposes to generate simple gene deletions or reporter gene "knock-ins." The second method, ends-in targeting, targets a wild-type gene with an engineered mutated copy and generates a duplication structure at the target locus. This duplication can subsequently be reduced to one copy, removing the wild-type gene and leaving only the introduced mutation. Although more complicated in the cloning and genetic manipulations (see Note 1), this approach has the benefit that the mutations may be introduced with no other remnant of the targeting procedure. This "surgical" approach will appeal to investigators who desire minimal perturbation to the genome, such as single nucleotide mutation. Although both approaches appear to be approximately equally efficient (see Note 2), each method has separate strengths and drawbacks. The choice of which approach is best depends on the researcher's goal.
• Goll, M. G., Kirpekar, F., Maggert, K. A., Yoder, J. A., Hsieh, C., Zhang, X., Golic, K. G., Jacobsen, S. E., & Bestor, T. H. (2006). Methylation of tRNAAsp by the DNA methyltransferase homolog Dnmt2. Science (New York, N.Y.), 311(5759), 395-8.
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  The sequence and the structure of DNA methyltransferase-2 (Dnmt2) bear close affinities to authentic DNA cytosine methyltransferases. A combined genetic and biochemical approach revealed that human DNMT2 did not methylate DNA but instead methylated a small RNA; mass spectrometry showed that this RNA is aspartic acid transfer RNA (tRNA(Asp)) and that DNMT2 specifically methylated cytosine 38 in the anticodon loop. The function of DNMT2 is highly conserved, and human DNMT2 protein restored methylation in vitro to tRNA(Asp) from Dnmt2-deficient strains of mouse, Arabidopsis thaliana, and Drosophila melanogaster in a manner that was dependent on preexisting patterns of modified nucleosides. Indirect sequence recognition is also a feature of eukaryotic DNA methyltransferases, which may have arisen from a Dnmt2-like RNA methyltransferase.
• Maggert, K. A., & Golic, K. G. (2005). Highly efficient sex chromosome interchanges produced by I-CreI expression in Drosophila. Genetics, 171(3), 1103-14.
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  The homing endonuclease I-CreI recognizes a site in the gene encoding the 23S rRNA of Chlamydomonas reinhardtii. A very similar sequence is present in the 28S rRNA genes that are located on the X and Y chromosomes of Drosophila melanogaster. In this work we show that I-CreI expression in Drosophila is capable of causing induced DNA damage and eliciting cell cycle arrest. Expression also caused recombination between the X and Y chromosomes in the heterochromatic regions where the rDNA is located, presumably as a result of a high frequency of double-strand breaks in these regions. Approximately 20% of the offspring of males expressing I-CreI showed exceptional inheritance of X- and Y-linked markers, consistent with chromosome exchange at rDNA loci. Cytogenetic analysis confirmed the structures of many of these products. Exchange between the X and Y chromosomes can be induced in males and females to produce derivative-altered Y chromosomes, attached-XY, and attached-X chromosomes. This method has advantages over the traditional use of X rays for generating X-Y interchanges because it is very frequent and it generates predictable products.
• Maggert, K. A., & Golic, K. G. (2002). The Y chromosome of Drosophila melanogaster exhibits chromosome-wide imprinting. Genetics, 162(3), 1245-58.
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  Genomic imprinting is well known as a regulatory property of a few specific chromosomal regions and leads to differential behavior of maternally and paternally inherited alleles. We surveyed the activity of two reporter genes in 23 independent P-element insertions on the heterochromatic Y chromosome of Drosophila melanogaster and found that all but one location showed differential expression of one or both genes according to the parental source of the chromosome. In contrast, genes inserted in autosomal heterochromatin generally did not show imprint-regulated expression. The imprints were established on Y-linked transgenes inserted into many different sequences and locations. We conclude that genomic imprinting affecting gene expression is a general property of the Drosophila Y chromosome and distinguishes the Y from the autosomal complement.
• Maggert, K. A., & Karpen, G. H. (2001). The activation of a neocentromere in Drosophila requires proximity to an endogenous centromere. Genetics, 158(4), 1615-28.
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  The centromere is essential for proper segregation and inheritance of genetic information. Centromeres are generally regulated to occur exactly once per chromosome; failure to do so leads to chromosome loss or damage and loss of linked genetic material. The mechanism for faithful regulation of centromere activity and number is unknown. The presence of ectopic centromeres (neocentromeres) has allowed us to probe the requirements and characteristics of centromere activation, maintenance, and structure. We utilized chromosome derivatives that placed a 290-kilobase "test segment" in three different contexts within the Drosophila melanogaster genome--immediately adjacent to (1) centromeric chromatin, (2) centric heterochromatin, or (3) euchromatin. Using irradiation mutagenesis, we freed this test segment from the source chromosome and genetically assayed whether the liberated "test fragment" exhibited centromere activity. We observed that this test fragment behaved differently with respect to centromere activity when liberated from different chromosomal contexts, despite an apparent sequence identity. Test segments juxtaposed to an active centromere produced fragments with neocentromere activity, whereas test segments far from centromeres did not. Once established, neocentromere activity was stable. The imposition of neocentromere activity on juxtaposed DNA supports the hypothesis that centromere activity and identity is capable of spreading and is regulated epigenetically.
• Maggert, K. A., & Karpen, G. H. (2000). Acquisition and metastability of centromere identity and function: sequence analysis of a human neocentromere. Genome research, 10(6), 725-8.
• Dobie, K. W., Hari, K. L., Maggert, K. A., & Karpen, G. H. (1999). Centromere proteins and chromosome inheritance: a complex affair. Current opinion in genetics & development, 9(2), 206-17.
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  Centromeres and the associated kinetochores are involved in essential aspects of chromosome transmission. Recent advances have included the identification and understanding of proteins that have a pivotal role in centromere structure, kinetochore formation, and the coordination of chromosome inheritance with the cell cycle in several organisms. A picture is beginning to emerge of the centromere-kinetechore as a complex and dynamic structure with conservation of function at the protein level across diverse species.
• Maggert, K., Levine, M., & Frasch, M. (1995). The somatic-visceral subdivision of the embryonic mesoderm is initiated by dorsal gradient thresholds in Drosophila. Development (Cambridge, England), 121(7), 2107-16.
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  The maternal dorsal regulatory gradient initiates the differentiation of the mesoderm, neuroectoderm and dorsal ectoderm in the early Drosophila embryo. Two primary dorsal target genes, snail (sna) and decapentaplegic (dpp), define the limits of the presumptive mesoderm and dorsal ectoderm, respectively. Normally, the sna expression pattern encompasses 18-20 cells in ventral and ventrolateral regions. Here we show that narrowing the sna pattern results in fewer invaginated cells. As a result, the mesoderm fails to extend into lateral regions so that fewer cells come into contact with dpp-expressing regions of the dorsal ectoderm. This leads to a substantial reduction in visceral and cardiac tissues, consistent with recent studies suggesting that dpp induces lateral mesoderm. These results also suggest that the dorsal regulatory gradient defines the limits of inductive interactions between germ layers after gastrulation. We discuss the parallels between the subdivision of the mesoderm and dorsal ectoderm.
• Ip, Y. T., Maggert, K., & Levine, M. (1994). Uncoupling gastrulation and mesoderm differentiation in the Drosophila embryo. The EMBO journal, 13(24), 5826-34.
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  In Drosophila, ventral furrow formation and mesoderm differentiation are initiated by two regulatory genes, twist (twi) and snail (sna). Both genes are evolutionarily conserved and have also been implicated in vertebrate gastrulation. Evidence is presented that sna is sufficient to initiate the invagination of the ventral-most embryonic cells in the absence of twi+ gene activity. The invaginated cells fail to express mesoderm regulatory genes, suggesting that ventral furrow formation can be uncoupled from mesoderm differentiation. Despite the previous demonstration that sna functions as a sequence-specific transcriptional repressor, low levels of sna that fail to repress neuroectoderm determinants in the presumptive mesoderm are nonetheless able to promote invagination. Cells that possess an ambiguous developmental identity can initiate the invagination process, providing further evidence that ventral furrow formation need not be linked to mesoderm differentiation.
• Taiz, L., Nelson, H., Maggert, K., Morgan, L., Yatabe, B., Taiz, S. L., Rubinstein, B., & Nelson, N. (1994). Functional analysis of conserved cysteine residues in the catalytic subunit of the yeast vacuolar H(+)-ATPase. Biochimica et biophysica acta, 1194(2), 329-34.
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  The A subunit of the yeast vacuolar ATPase contains three highly conserved cysteines: Cys-261, Cys-284, and Cys-538. Cys-261 is located within the nucleotide-binding P-loop. Each of the conserved cysteines, and one nonconserved cysteine, Cys-254, were altered to serine by site-directed mutagenesis, and the effects on growth at pH 7.5 were determined. The Cys-254-->Ser, Cys-261-->Ser and the double mutants all grew at pH 7.5 and contained nitrate- and bafilomycin-sensitive ATPase activity. However, the ATPase activities of the Cys-261-->Ser and the double mutants were insensitive to the sulfhydryl group inhibitor, N-ethylmaleimide, demonstrating that Cys-261 is the site of inhibition by N-ethylmaleimide. Changing either Cys-284 or Cys-538 to serine prevented growth at pH 7.5. Cys-284 and Cys-538 thus appear to be essential cysteine residues which are required either for assembly or catalysis.

Presentations

• Maggert, K. (2021, April). Epigenetics: not as epi- as we thought. University of Alabama – Birmingham. University of Alabama – Birmingham.
• Maggert, K. (2021, June). Rethinking Epigenetics: are we stuck at a roadblock that doesn’t exist?. High-Risk High-Reward Symposium. National Institutes of Health.
• Maggert, K. (2021, March). Epigenetic Instability. Genome Instability Working Group. University of Arizona.
• Maggert, K. (2021, November). Live Monitoring of Heterochromatic Gene Silencing. "111 Event" for studies of Chromatin Structure and Function. Hengyang College of Medicine, University of South China.
• Maggert, K. (2021, October). Bloom Syndrome and Ribosomal DNA Instability: transgenerational effects. Emerging Roles for the Nucleolus. Online Symposium.
• Maggert, K. (2020, April). Epigenetics: not as epi- as we thought. CMM departmental seminar. University of Arizona.
• Maggert, K. (2020, April). ins – wtf?. UACC genomic instability working group seminar. University of Arizona.
• Maggert, K. (2020, February). Epigenetics: not as epi- as we thought. MCB departmental seminar. University of Arizona.
• Maggert, K. (2019, July). Heterochromatin-induced Gene Silencing is Decided Early and Set Late. Drosophila Heterochromatin Meeting. Spoleto, Italy.
• Maggert, K. (2017, June). Accessing the timing and stability of epigenetic silencing. Epigenetics Gordon Research Conference. Holderness, New Hampshire: Gordon Conference.
• Maggert, K. (2017, October). rDNA as a genetic modifier: rethinking the idea of epigenetic modification. Emerging Roles for the Nucleolus. Stowers Institute, Kansas City, Missouri: American Society for Biochemistry and Molecular Biology.

Poster Presentations

• Maggert, K. (2017, April). Heterochromatin-induced Gene Silencing is Decided Early and Set Late. Annual Drosophila Research Conference. San Diego, California: Genetics Society of America.