Andreas Heyland

Dr. Andreas Heyland

orcid

Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 October 2006 in Nature
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Journal Article
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SBSarah J. Bourlat
Sarah J. Bourlat
TJThorhildur Juliusdottir
Thorhildur Juliusdottir
CLChristopher J. Lowe
Christopher J. Lowe
RFRobert Freeman
Robert Freeman
JAJochanan Aronowicz
Jochanan Aronowicz
MTMaximilian J. Telford
Maximilian J. Telford

1 December 2006 in Cell
Verified
Journal Article
Closed access
LMLeonid L. Moroz
Leonid L. Moroz
JEJohn R. Edwards
John R. Edwards
SPSathyanarayanan V. Puthanveettil
Sathyanarayanan V. Puthanveettil
AKAndrea B. Kohn
Andrea B. Kohn
THThomas Ha
Thomas Ha
EKEric R. Kandel
Eric R. Kandel

15 August 2008 in Journal of Experimental Biology
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Journal Article
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TFThomas Flatt
Thomas Flatt
AHAndreas Heyland
Andreas Heyland
FRFlorentina Rus
Florentina Rus
EPErmelinda Porpiglia
Ermelinda Porpiglia
CSChris Sherlock
Chris Sherlock
NSNeal Silverman
Neal Silverman
SUMMARY Juvenile hormone (JH) and 20-hydroxy-ecdysone (20E) are highly versatile hormones, coordinating development, growth, reproduction and aging in insects. Pulses of 20E provide key signals for initiating developmental and physiological transitions, while JH promotes or inhibits these signals in a stage-specific manner. Previous evidence suggests that JH and 20E might modulate innate immunity, but whether and how these hormones interact to regulate the immune response remains unclear. Here we show that JH and 20E have antagonistic effects on the induction of antimicrobial peptide (AMP) genes in Drosophila melanogaster. 20E pretreatment of Schneider S2* cells promoted the robust induction of AMP genes, following immune stimulation. On the other hand, JH III, and its synthetic analogs (JHa) methoprene and pyriproxyfen, strongly interfered with this 20E-dependent immune potentiation, although these hormones did not inhibit other 20E-induced cellular changes. Similarly, in vivo analyses in adult flies confirmed that JH is a hormonal immuno-suppressor. RNA silencing of either partner of the ecdysone receptor heterodimer (EcR or Usp) in S2* cells prevented the 20E-induced immune potentiation. In contrast, silencing methoprene-tolerant (Met), a candidate JH receptor, did not impair immuno-suppression by JH III and JHa, indicating that in this context MET is not a necessary JH receptor. Our results suggest that 20E and JH play major roles in the regulation of gene expression in response to immune challenge.

11 October 2006 in Integrative and Comparative Biology
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Journal Article
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CBC. D. Bishop
C. D. Bishop
DED. F. Erezyilmaz
D. F. Erezyilmaz
TFT. Flatt
T. Flatt
Christos GeorgiouChristos Georgiou
Christos Georgiou
MHM. G. Hadfield
M. G. Hadfield
JYJ. H. Youson
J. H. Youson
Metamorphosis (Gr. meta- “change” + morphe “form”) as a biological process is generally attributed to a subset of animals: most famously insects and amphibians, but some fish and many marine invertebrates as well. We held a symposium at the 2006 Society for Integrative and Comparative Biology (SICB) annual meeting in Orlando, FL (USA) to discuss metamorphosis in a comparative context. Specifically, we considered the possibility that the term “metamorphosis” could be rightly applied to non-animals as well, including fungi, flowering plants, and some marine algae. Clearly, the answer depends upon how metamorphosis is defined. As we participants differed (sometimes quite substantially) in how we defined the term, we decided to present each of our conceptions of metamorphosis in 1 place, rather than attempting to agree on a single consensus definition. Herein we have gathered together our various definitions of metamorphosis, and offer an analysis that highlights some of the main similarities and differences among them. We present this article not only as an introduction to this symposium volume, but also as a reference tool that can be used by others interested in metamorphosis. Ultimately, we hope that this article—and the volume as a whole—will represent a springboard for further investigations into the surprisingly deep mechanistic similarities among independently evolved life cycle transitions across kingdoms.

11 October 2006 in Integrative and Comparative Biology
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AHAndreas Heyland
Andreas Heyland
LMLeonid L. Moroz
Leonid L. Moroz
Metamorphosis in many animal groups involves a radical transition from a larval to a juvenile/adult body plan and the challenge of orchestrating 2 overlapping developmental programs simultaneously, that is, larval development and juvenile development. Metamorphic competence directly precedes this radical change in morphology and can be best described as the developmental potential of a larva to undergo the radical transition in response to internal or external signals. Several studies have employed genomic approaches (for example, microarrays or subtractive hybridization methods) to gain insights into the complexity of changes in gene expression associated with metamorphic transitions. Availability of this technology for an increasing number of organisms from diverse taxonomic groups expands the scope of species for which we can gain detailed understanding of the genetic and epigenetic architecture underlying metamorphosis. Here, we review metamorphosis in insects, amphibians, and several marine invertebrate species including the sea hare Aplysia californica and summarize mechanisms underlying the transition. We conclude that all metamorphoses share at least 4 components: (1) the differentiation of juvenile/adult structures, (2) the degeneration of larval structures, (3) metamorphic competence, and (4) change in habitat. While transcription levels detected by microarray or other molecular methods can vary significantly, some similarities can be observed. For example, transcripts related to stress response, immunity, and apoptosis are associated with metamorphosis in all investigated phyla. It also appears that signaling mediated by hormones and by nitric oxide can contribute to these stress-related responses and that these molecules can act as regulators of metamorphic transitions. This might indicate either that all of these distantly related organisms inherited the same basic regulatory machinery that was employed by their most recent common ancestor (RCA) in orchestrating life history transitions. Alternatively, these regulatory modules may have been used by the RCA for other purposes and have been independently co-opted to regulate metamorphic transitions in a variety of distantly related animals. We propose that such instances of independent origin or homoplasy in the evolution of metamorphosis might have resulted from specific constraints in signal transduction pathways. Modern genomic tools can help to further explore homoplastic signaling modules when used in a comparative context.

1 December 2005 in Journal of Experimental Biology
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AHAndreas Heyland
Andreas Heyland
LMLeonid L. Moroz
Leonid L. Moroz
SUMMARY: Thyroid hormones (THs) are small, lipophilic signaling molecules built from tyrosine and iodine. TH action is well characterized in vertebrates, where these molecules play a fundamental role as regulators of development,metabolism, growth and differentiation. Increasing evidence suggests that THs also function in a variety of invertebrate species. Two alternative sources of hormone for animals are exogenous (from food items) and endogenous synthesis. We propose that exogenous THs can convey environmental information as well as regulate metabolism, revealing new communication avenues between organisms from different kingdoms. While such modes of cross-kingdom communication have been previously considered for fatty acid-based signaling and steroid hormones in plant–animal interactions, this is the first attempt to explore such a mode of action for TH signaling. We suggest that exogenous sources of TH(from food) may have been ancestral, while the ability to synthesize TH endogenously may have evolved independently in a variety of metazoans,resulting in a diversity of signaling pathways and, possibly, morphological structures involved in TH-signaling.