Fordham University


 

  


Dr. Jason Z. Morris

Associate Professor of Biology
Department of Natural Sciences LL rm 813
Fordham College at Lincoln Center
New York, NY 10023
Office:817A


Email:

cjamorrisATfordham.edu




Subjects Taught at Fordham (2003-Present):

Genetics
Cell and Developmental Biology
Molecular Biology
Biomedical Informatics
Honors Natural Science I and II
Life Sciences Core Courses
Biomedical Informatics

 


Other Interests and Service:

        Fordham Hillel faculty advisor
        Pre-Medical/Health Professions Advising Committee



Education, Training, Awards, and Grants:

      

B.A. in biology: Yale University ‘91 (Summa cum laude, distinction in biology)
       Ph.D. in genetics: Harvard Medical School ‘97
       Post-doctoral Fellowship: Lehmann Laboratory, Skirball Institute of Biomolecular Medicine ’97-‘03     

2011 Fordham University Teaching Award in the Natural and Life Sciences
2011 Fordham-Funded Research Scholar Award

Fellowship Funding:

              American Cancer Society, Howard Hughes Medical Institute
       Principal Investigator External Funding:

              National Institutes of Health/National Institute of General Health and Medicine R15 Award GM090173-01 for Molecular Identification and Functional Characterization of fried, a Gene Required for Growth and Fertility in Drosophila 2010-2013
              National Institutes of Health/National Institute of General Health and Medicine R15 Award GM074735-01 for Characterization and Molecular Identification of Benedict, a regulator of Drosophila Endoreplication: 2005-2008




Research Projects:

Ph.D. thesis: Cloning and characterization of the gene age-1, a regulator of life span and developmental response to crowding and starvation in C. elegans. AGE-1 functions in the same pathway as insulin receptor. Low AGE-1 function increases life span. When C. elegans is starved and overcrowded, AGE-1 is off. As a result, the worm arrests development and ages very slowly until conditions improve. 

Post-doctoral research:
          A) Cloning and characterization of the gene twin, which is necessary for Drosophila oogenesis (production of egg cells). Twin regulates the length of poly(A) tails on certain mRNAs in the fruit fly ovary. Without Twin, cells in the ovary do not progress through the cell cycle properly and cannot develop as oocytes (eggs).

          B) Identification of eight novel genes that are required for early oogenesis, including benedict (bene) and fried, which are my current areas of focus (see below).

Current research:
          My general area of interest is the genetic control of development-- how genes build a complex organism with many very different cell types from a single cell, the fertilized egg.

          My laboratory’s long-term goal is to improve our understanding of growth and cell cycle regulation during Drosophila development. I have guided over 20 Fordham undergraduates in independent research on these projects and many of them have co-authored articles and/or presentations at national and international meetings (see Publications and Presentations below). We are currently working on several projects:

1)  cloning and characterization of bene/gatA:  My collaborators and I discovered bene in a clonal screen in the female germline while I was a post-doctoral fellow at the Skirball Institute of Biomolecular Medicine at NYU Medical Center. We showed that bene/gatA mutants have characteristic ovary defects that suggest the gene is important for regulating the Drosophila endocycle and for maintaining proper chromosome morphology in nurse cells and oocytes during oogenesis (Morris, et al, ’03, Morris, et al, '08, Figures 1 and 2). 

2) In 2005, we published a paper (Morris, et al, ’05) on the cloning of twin, a gene required for normal cell cycle control during oogenesis.  In that paper, I showed that twin mutants mis-regulate the cell cycle control gene, cyclin A, because of a defect in mRNA poly(A) tail deadenylation.

3) We have also mapped mutations in fried, another mutant uncovered in the oogenesis screen, to a small region (approximately 4-6 candidate genes) on chromosome 3. These mutants have larval and oogenesis defects similar to those found in bene/gatA mutants. We are currently sequencing candidate genes in our fried mutants strains and phenotypically characterizing these mutants.

 Opportunities for Undergraduate Research
          My lab offers many opportunities for undergraduates who would like to receive training in genetics, molecular biology, cell biology, and developmental biology.

          Stipends for summer research students are available on a competitive basis from my grant and from the Department of Natural Sciences, through the Ambrose Fund. Additional information and application forms are available from the Department Chairperson (LL 813).

 

Figure 1

Figure 1: bene/gatA growth and maturation defects. All larvae are siblings hatched from eggs collected from the same vial after a two-hour egg-lay. (A) gatA larvae are much smaller than wild type five days AEL. Left, gatA/+. Right gatA112/Df. (B) Graph showing delayed molting into third instar larvae of gatA mutants. Left, gatA/+. Right, gatA112/Df. 
(C, D, E) mouth hook morphology 5 days AEL. (C) wild type  third instar larva. (D) gatA112/Df second instar larva (E) gatA112/Df third instar larva.

 

Figure 2

Figure 2: Mosaic analysis and expression of bene/gatA.  w, ey-FLP, Gla-lacZ; FRT Rps3, P{ubi-GFP, w+}/TM6B females were crossed by FRT e gatA50/TM3, Sb males, FRT e gatA112/TM3, Sb males, or FRT +/TM3, Sb males. (A-H) photographs of adult eyes. The FRT Rps3 chromosome carries a w+ transgene. Rps3 is recessive cell lethal. So in males, cells that have not undergone recombination are yellow. Cells that have recombined are white (homozygous for + or gatA, depending on the cross). (A, B, E, F): female eyes are w+, aiding phenotypic analysis, but making it difficult to determine the genotype of cells. (C, D, G, H): male eyes are w- , permitting easy genotyping of eye clones. (A) Wild type clone shows normal growth and development. (B) Rps3/+ eyes (no clones induced) are slightly smaller than wild type. (C) gatA112/+ eyes (no clones induced) and (G) gatA50/+ eyes (no clones induced) are normal. (D,E,F) gatA112 clones and (H) gatA50 clones cause small, misshapen eyes with cuticle scars and ectopic bristles.  There is a small, pale yellow region in the upper portion of the eye in (D), because ey-FLP induced mitotic recombination somewhat late in this eye.  I) RTPCR of gatA from RNA extracts from larval: gut (lanes 1,2), imaginal discs (lanes 3,4), fat body (lanes 5,6), salivary gland

 

Publications and Presentations:

Publications:
  • Morris, JZ, Kruyer, A, Bergman L, Moffitt O, Siletti K, McCord ,Persky R. Drosophila gatA mutants mistranslate the mitochondrial genome, up-regulate AMPK, and down-regulate S6 Kinase to arrest larval growth. In Preparation.

  • Morris, JZ. Substance ontology cannot determine the moral status of embryos. Journal of Medicine and Philosophy: In Press.

  • Morris, JZ, Bergman L, Kruyer A, Guigova A, Gertsberg M, Arias R, Pogorzelska M. 2008. Mutations in the Drosophila mitochondrial tRNA amidotransferase, bene/gatA, cause growth defects in mitotic and endoreplicating tissues . Genetics 178: 979-987.

  • Morris JZ, Hong, A, Lilly, M, and   Lehmann R. twin, a CCR4 homolog, regulates cyclin poly(A) tail length to permit Drosophila oogenesis.  Development: 132: 1165-1174.

  • Morris, JZ, Navarro C, Lehmann R.  2003.  Identification and characterization of novel genes required for oocyte specification in Drosophila. Genetics 164: 1435-1446.

  • Navarro C, Lehmann R, Morris J.  2001.  Oogenesis: Setting one sister above the rest.  Current Biology 11: R162-R165.

  • Morris J, Lehmann R, Navarro, C. 2000.  PARallels in axis formation.  Science 288: 1759-1760.

  • Morris J, Lehmann R. 1999.  Drosophila oogenesis: Versatile spn doctors.  Current Biology 9: R55-R58.

  • Morris JZ, Tissenbaum HA, Ruvkun G.  1996. The C. elegans phosphatidylinositol 3-kinase homologue, AGE-1, regulates longevity and diapause arrest.  Nature 382: 536-539.


Presentations:

  • Morris, JZ. “Identification and analysis of genes required for Drosophila oogenesis and growth.” Fordham College at Rose Hill Biology Lecture, Bronx, NY, March 2011.

  • Carlisdania Mendoza, Guarav Saharia, Lillian Chiu, Alison E. Lindsay, Jason Morris. “Genotypic and phenotypic characterization of the Drosophila mutant, fried.” 51st Annual Drosophila Research Conference, San Diego, CA, March 2011.

  • Jason Z. Morris and Jennifer Ma. “fried mutants exhibit defects in oogenesis and larval and pupal development.”  Cell Cycle Meeting, Cold Spring Harbor, NY, May 2010.

  • Kimberly Siletti, Thomas McCord, Anna Kruyer, Leah Bergman, Olivia Moffitt, Christopher O’Connor, Jane Mueller, Joseph Carnevale, Rebecca Persky and Morris, JZ. “Analysis of the biochemical and cellular defects caused of gatA loss-of-function mutants in Drosophila larvae.” 49th Annual Drosophila Research Conference, Chicago, IL, March 2009.

  • Thomas McCord, Kimberly Siletti, Rebecca Persky and Morris, JZ. “Mapping and analysis of fried, a gene required for egg chamber maturation, larval growth and puparial development.” 49th Annual Drosophila Research Conference, Chicago, IL, March 2009.

  • Morris, JZ. “Development in model systems and the study of human disease.” College at 60 Lecture, Fordham University, December, 2008.

  • Morris, JZ. “Drosophila growth and oogenesis genes.” Department of Cell Biology, Massachusetts General, Boston, MA, October 2008.

  • Morris, JZ. “Identification and analysis of genes required for Drosophila growth and oogenesis.” Skirball Institute of Biomolecular Medicine / NYU Medical College, NY, NY, July 2008.

  • Anna Kruyer, Leah Bergman, Olivia Moffitt, Adriana Guigova, Mikhail Gertsberg, Ronald Arias, Monika Pogorzelska, Vanessa Flores, Jane Mueller, Christopher O’Connor, Grace Vernon, and Jason Morris “Analysis of growth defects caused by loss-of-function of gatA, a gene required for growth and maturation in Drosophila.” Independent Sector Undergraduate Research Exposition, Albany, NY, January 2008.

  • Bergman, L, Kruyer, A, Gertsberg, M, Guigova, A, and Morris, JZ. “Genetic analysis of gatA, a glutamyl-tRNA (Gln) amidotransferase homolog required for growth and maturation in Drosophila.” Einsteins in the City International Undergraduate Research Conference, New York, NY, October 2007.

  • Moffitt, O, Andreyeva, A, Bergman, L, Kruyer, A, and Morris, JZ. “Molecular and biochemical analysis of the function of gatA, a gene required for growth and maturation in Drosophila.” Einsteins in the City International Undergraduate Research Conference, New York, NY, October 2007.

  • Mueller, J, O’Connor, C, Vernon, G, and Morris, JZ. “Analysis of growth defects caused by loss-of-function of gatA, a gene required for growth and maturation in Drosophila. Einsteins in the City International Undergraduate Research Conference, New York, NY, October 2007.

  • Bergman, L, Kruyer, A, Gertsberg, M, Guigova, A, and Morris, JZ. “Genetic and molecular analysis of bene, a glutamyl-tRNA (Gln) amidotransferase homolog required for growth and maturation in Drosophila.” 48th Annual Drosophila Research Conference, Philadelphia, PA, March 2007.

  • Kruyer, A, Bergman, L, Gertsberg, M, Vernon, G, and Morris, JZ. “Molecular, cellular and biochemical analysis of the function of bene/gatA, a gene required for growth and maturation in Drosophila.” 48th Annual Drosophila Research Conference, Philadelphia, PA, March 2007.

  • Morris, JZ.  “Growth and cell cycle mutants in Drosophila.” Columbia College of Physicians and Surgeons, NY, NY: October, 2006.

  • Morris, JZ, Gertsberg, M, Guigova, A, Arias, A, Flores, V, and Pogorszelska, M. “Mutations in benedict cause defects in the larval and adult endocycle and in nurse cell and oocyte chromosome morphology in Drosophila.”  Cell Cycle Meeting, Cold Spring Harbor, NY: May 2006.

  • Morris, JZ. “The genetic revolution: organisms by design.” College at 60 Lecture, Fordham University, November, 2004.

  • Morris JZ, Hong, A, Lilly, M, and Lehmann R. “twin, a CCR4 homolog, regulates cyclin poly(A) tail length to permit Drosophila oogenesis.”  Germ Cell Meeting, Cold Spring Harbor, NY:  October, 2004.

  • Morris, JZ. “Developmental Genetics Research—questions and approaches.” Seminar for Science Research Training Program, New York Academy of Science, New York, NY: June 24, 2004.

  • Morris, JZ. “A View From Just Over The Wall—pursuing a career as a science professor at a primarily undergraduate institution.”  Seminar for Future Science Educators at The Sackler Institute, New York University Medical Center, New York, NY: March 2, 2004.

  • Morris, JZ, Navarro, C, Hong, A, Lilly, M, and Lehmann, R. “A Genetic Analysis of Drosophila Egg Chamber Development.”  Lehigh University, Bethlehem, PA: Februrary, 2003.

  • Morris, JZ. “Perspectives on Genetic Engineering.” Fordham University at Lincoln Center, NY: February, 2003

  • Morris, JZ, Navarro, C, Hong, A, Lilly, M, and Lehmann, R. “Genetics of Egg Chamber Development in Drosophila.”  Swarthmore College, Swarthmore, PA:  February, 2003.

  • Morris, JZ, Navarro, C, Hong, A, Lilly, M, and Lehmann, R “A Genetic Analysis of Egg Chamber Development in Drosophila.”  CUNY Baruch College, NY: January, 2003.

  • Morris JZ, Hong, A, Lilly, M, and Lehmann R. “Cloning and characterization of twin, a ccr4 homolog required for Drosophila oocyte specification and egg chamber development.”  Germ Cell Meeting, Cold Spring Harbor, NY:  October, 2002.

  • Morris, JZ, Navarro, C, and Lehmann, R.  “Isolation and analysis of bob, Doa, and eight new genes required for early Drosophila oogenesis.” Germ Cell Meeting, Cold Spring Harbor, NY:  October 2002.

  • Morris, JZ, and Lehmann, R “twin/Dccr4 and early Drosophila oogenesis.”  NIH/NICHD, Bethesda, MD:  July 2001.

  • Morris, JZ and Lehmann, R. “Identification and characterization of oogenesis mutants.” 41st Annual Drosophila Research Conference, Pittsburgh, PA:  March  2000.

  • Morris, JZ and Lehmann, R. “Oocyte / nurse cell development in the Drosophila germline cyst.” 39th Annual Drosophila Research Conference.  Washington, D.C:  March, 1998.

  • Morris, JZ, Tissenbaum, H, and Ruvkun, G. “The C. elegans phosphatidylinositol 3-kinase homologue age-1 regulates dauer arrest and senescence”  East Coast Worm Meeting. New Brunswick, NJ:  June, 1996.

  • Morris, JZ and Ruvkun, G. “Mapping and cloning daf-23.”  International Worm Meeting, Madison, WI:  June, 1995.
 

 

 

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