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School of Biological Sciences

School of Biological Sciences Seminars

May 1 at 4:00 in MLT 210 Dr. John Gustafson of OK State Univ

GustafsonMy journey with an antimicrobial resistance clone of Staphylococcus aureus.

Vancomycin for years has been an effective agent for the treatment of multiple antibiotic resistant strains of Staphylococcus aureus, more commonly referred to as methicillin-resistant S. aureus or MRSA. The use of vancomycin increased greatly as infections caused by MRSA increased and it is now obvious that natural selection took over. For the past 11 years of my career I have been elucidating a mechanism leading to the expression of a reduced vancomycin susceptibility mechanism in S. aureus. The vancomycin-reduced susceptibility mechanism being investigated is expressed by S. aureus strain MM66, which our laboratory isolated from a Las Cruces New Mexico hospital patient in 2003. MM66 is a hetero-vancomycin-intermediate S. aureus (hVISA) strain that appears vancomycin-susceptible during standard minimum inhibitory concentration analysis, yet harbors a stable vancomycin-intermediate S. aureus (VISA) subpopulation(s) able to grow on relatively high vancomycin concentrations. To date, this work has uncovered all the mutations associated the MM66 hVISA phenotype, and mutations that lead to the formation of MM66 VISA mutants. Experiments were also performed to confirm hypotheses that link MM66 VISA mutations and transcriptional alterations to altered whole cell autolysis associated with the VISA mechanism. Mutational and transcriptional data also led to lines of experimentation to determine additional phenotypic alterations associated with the MM66 VISA mutants. Another project investigating the epidemiology of S. aureus strains causing bovine mastitis in a dairy 17 miles from Las Cruces uncovers a strain (H29) with a tight familial relationship to MM66 and another strain that killed a patient suffering from endocarditis. My journey with these S. aureus clones concludes with a clearer understanding of the power modern genomics provides to scientists working on antimicrobial resistance and pathogen epidemiology.

April 24 at 4:00 in MLT 210 – Dr. Murat Bastepe of Harvard Univ. Medical School

Murat BStimulatory G protein alpha-subunit (Gsα) and its variant XLαs in the development of endocrine of bone disease.

The stimulatory G protein mediates the actions of numerous hormones, neurotransmitters, and autocrine/paracrine factors through generation of the intracellular second messenger cyclic AMP (cAMP).  The alpha subunit of the stimulatory G protein (Gsα) is encoded by the GNAS complex locus, which gives rise to several additional products including the extra-large Gsα variant XLαs.  Mutations in GNAS lead to various human diseases.  Inactivating mutations of this gene cause Albright’s hereditary osteodystrophy and, when inherited maternally, end-organ resistance to parathyroid hormone (PTH).  Somatic or post-zygotic mutations leading to constitutive Gsα and XLαs activity are found in various endocrine and non-endocrine tumors, fibrous dysplasia of bone, and McCune-Albright syndrome.  GNAS has a complex parent-of-origin specific expression profile.  Gsα is biallelically expressed in most tissues, but the expression from its paternal allele is silenced in a small set of tissues, such as pituitary and renal proximal tubules.  In contrast, XLαs expression is paternal in nearly all tissues thus far investigated; one exception is clonal human bone marrow stromal cells, in which biallelic XLαs expression was documented.  Most of the disease-causing GNAS mutations alter the activity of not only Gsα but also XLαs, particularly when they are located on the paternal allele.  However, the role of XLαs and its involvement in the pathogenesis of diseases caused by GNAS mutations are poorly defined.  Our lab has been investigating this question over the past several years.  We have shown that XLαs can mimic Gsα when overexpressed in cultured cells or in transgenic mice.  We have also shown that inactivating GNAS mutations affect both XLαs and Gsα in the same manner.  However, we revealed some distinctions between XLαs and Gsα at the molecular level.  Our biochemical and molecular studies revealed that XLαs differs from Gsα in its subcellular trafficking, and that it is more potent than Gsα with respect to basal cAMP generation.  Our results also suggest that XLαs, but not Gsα, can prolong the signaling of the PTH receptor in transfected cells.  In addition, we studied the possible involvement of constitutive XLαs activity in the pathogenesis of McCune-Albright syndrome.  A constitutively active XLαs mutant found in these patients was found to generate stronger basal cAMP signaling and to inhibit differentiation of preosteoblastic MC3T3E1 cells more significantly than the cognate Gsα mutant.  Furthermore, we analyzed biopsy samples from several patients with this disorder and showed that the activating GNAS mutation is present on the paternal allele in some, but not all, cases.  Our results also demonstrated that constitutive XLαs activity can lead to thyrotoxicity and ovarian cysts, two of the multiple findings of McCune-Albright syndrome, in the absence of constitutive Gsα activity.  Thus, our investigations indicate that XLαs is a potent cAMP generating signaling protein that is distinct from Gsα in certain aspects.  It appears that altered XLαs activity, along with altered Gsα activity, plays important roles in GNAS-related human diseases.  More recently, we have shown that loss of XLαs imprinting, which results in XLαs overexpression, leads to hypoglycemia and early postnatal lethality in a mouse model in which a region of the GNAS gene was deleted in order to model pseudohypoparathyroidism type Ib, a disorder caused by imprinting mutations of GNAS.  XLαs knockout mouse models, generated by others, also show hypoglycemia and early postnatal lethality, indicating that the level of XLαs has to be controlled carefully for survival after birth.   Furthermore, data from XLαs knockout mice suggest that XLαs has roles that are distinct from the roles of Gsα.  We are currently aiming to discover those unique XLαs actions in order to understand the relative significance of XLαs and Gsα in human physiology and disease.

Full School of Biological Sciences Seminar Schedule (pdf)

Seminars Archive

Integrative Biology Seminar Series

May 6 at noon in 121 slb – Keith Bowers

keith bMaternal immune stimulation and terminal investment in the house wren (Troglodytes aedon)

Full Schedule of the Integrative Biology Seminar Schedule (pdf)

Integrative Biology Seminar Archive

Molecular and Cellular Biology Seminar Series

April 23 at noon in 121 SLB Sarah Marrochello and Shawn Sternisha

MCBlogo2sm-cropSM Maternal antibody transfer in the red eared slider (Trachemys scripta)

SS Effects of rose bengal on Leishmania cells

April 16 at noon in 121 SLB – Samantha Atkinson

MCBlogo2sm-cropGenetic analysis of Ton2 dependent processes in microtubule organization in Arabidopsis

Full Molecular and Cellular Seminar Schedule (pdf)

Molecular and Cellular Seminar Archive

Welcome to the School of Biological Sciences

Craig Gatto, School Director

Whether you are interested in plants, animals, or microbes, our interdisciplinary and collaborative research groups in the School of Biological Sciences have something for you! From investigations involving interactions at subcellular molecular levels, to function and communication within/between organ systems and organisms, to evolutionary and ecological dynamics of populations, communities and ecosystems, see how ISU can set you on the right career path!

Biology News

David Borst Scholarship Winner – Marissa Cruz

borst scholarship winner 2014 smMarissa Cruz a senior in our school won the Borst Scholarship for her research in Wolfgang Stein lab. She is studying the long-term effects of Dopamine on the neurons that control the filtering of food in the crab, Cancer Borealis. As shown here she is able to monitor and quantify the activity of these neurons via extracellular recordings. Her research has led her to conclude that Dopamine not only has long-lasting effect but it is dependent on the presence of other neuromodulators.

Alumni Newsletter

Joe Kris and Jacob group photo smHere is the alumni newsletter for 2013/2014 academic year. Read about faculty’s and students’ research (shown here). Read about the tropical ecology class’ adventures. School of Biological Sciences 2014 Alumni Newsletter

Oral and Poster Winners from the Phi Sigma Research Symposium

Pegan Sauls smMany well-presented and informative posters and oral presentations were given as part of the 15th Phi Sigma Symposium. The winners for the best oral presentations were: Chris Loebach (first place), Keith Bowers (second) and Rachael Van Essen (third). The winners for the best poster presentations were: Pegan Sauls (first), Amanda Carter (second) and tied for third place – Austin Harvey and Marissa Cruz. Congratulations to the winners.


Biology from CASNews

Senior’s Next Stop is Medical School
Illinois State University senior Jacob Birlingmair and his faculty mentor R. K. Jayaswal.

Illinois State University senior Jacob Birlingmair and his faculty mentor R. K. Jayaswal.

Jacob Birlingmair, senior biology major, began applying to medical schools last summer with the help of his faculty mentor R. K. Jayaswal, who advised him through the process. Overall, Birlingmair was asked to be interviewed at 13 of the 17 programs that he applied to. One of the three schools that have already accepted him has offered to pay half his tuition.

Birlingmair assesses that it was his time spent with Jayaswal that really helped him move forward in becoming a doctor. He has worked within Jayaswal’s research lab for about two years.

To read more of this story, visit




Williams Wins Mercier Service Award
Ronald Williams

Ronald Williams

College of Arts and Sciences alumnus Dr. Ronald Williams was presented with the E. Burton Mercier Alumni Service Award for 2014 during the annual Founders Day convocation on February 20. Williams graduated with a degree in biology and went on to receive a medical degree from the University of Illinois.

Dr. Williams is a staff pediatrician at MultiCare in Olympia, Washington. A biology graduate, Williams earned a medical degree at the University of Illinois. He also completed a master’s in public health at Johns Hopkins University; a year at the U.S. Army War College in Pennsylvania; a Fellowship in Pediatric Infectious Disease; and a residency in Public Health and Preventive Medicine. He is American Board Certified in pediatrics and preventive medicine.

As the commanding officer of the U.S. Army Medical Research Institute of Infectious Disease, he studied the defense of infectious disease of biological weapons. He was also commanding officer of the General Leonard Wood Army Hospital and deputy director and chief of medicine at the Armed Forces Research Institute of Medical Science, Bangkok, Thailand.

Past director of health programs research for the Department of Defense, he was a member of the U.S delegation to the Third Review Conference of the Biological Weapons Convention in Geneva, Switzerland, during the Gulf War.

He and his wife offered medical aid in Sri Lanka following the tsunami. He has also overseen the medical needs of incarcerated youth and cared for Native Americans. Now retired from the military, he remains a practicing pediatrician.