Akshita Madala

Mentor: Dr. Clayton Mathews
College of Medicine
 
"As a high school student, I had the opportunity to gain a better understanding of the biomedical science field and conduct an independent research project in a university setting. Inspired by the challenging research process and eager to apply my academic knowledge, I became involved in a research lab as an undergraduate student. My research experience has allowed me to develop a strong foundation in genetics and pathology as well as an appreciation for the interdependence of clinical medicine and research."

Major

Microbiology & Cell Science

Minor

Health Disparities in Society

Research Interests

  • Type 1 Diabetes
  • Health Disparities
  • Arthritis

Academic Awards

  • University Scholars Program 2016
  • Cynthia W. Colangelo Award for Breast Cancer Awareness 2016
  • CLAS Dean's List
  • Honors Program

Organizations

  • RESULTS
  • Premed-American Medical Student Association (AMSA)
  • Community Health Service Corps (CHSC)

Volunteer

  • Mobile Outreach Clinic
  • Rahma Mercy Clinic
  • Project Downtown

Hobbies and Interests

  • Music
  • Baking
  • Art
  • Travelling

Research Description

Identification of the Genetic Mechanism of Idd22 Based Protection against Type 1 Diabetes
Type 1 Diabetes (T1D) is characterized by the progressive destruction of insulin-producing beta cells in pancreatic islets. The resulting insulin insufficiency requires life-long dependence on insulin therapy and maintenance of a healthy diet and lifestyle. Currently, this debilitating autoimmune disease has no known cure; therefore the need for alternative treatment options is necessary and urgent. Although it is a complex and multifactorial disease, T1D is largely driven by genetic mechanisms. Animal models have been extensively used to study the genetic and molecular mechanisms involved in T1D development. Specifically, our lab focuses on the ALR and NOD mouse models which demonstrate highly similar genomic backgrounds, however the ALR strain shows high resistance to spontaneous and induced T1D. Our studies have begun to provide insight into the specific loci that are responsible for the ALR’s genetic resistance against T1D. My project will focus on the highly protective locus that mapped to Chromosome (Chr) 8, and has been termed Insulin-dependent diabetes 22 (Idd22). In Dr. Mathews’ Lab, my aim is to fine map the Idd22 region and thus identify the gene(s) that confers resistance. Using the whole genome sequences, regions of interest can be compared by identifying possible single nucleotide polymorphisms (SNPs). Using primer design, PCR, and Sanger sequencing we can then validate the potential SNPs. By applying a bioinformatics approach, a SNP array will be developed. This SNP array will be used to analyze the NOD, ALR, and NOD-Idd22 congenic lines to identify candidate genes that will be tested for their ability to protect against T1D. By fine-mapping the Idd22 region, we hope to gain a better understanding of the protective mechanism, identify the T1D resistance allele and then determine if this region may also be important in human T1D.